A Study About The Changes in Levels of Pancreatic Enzymes in Cases of Chronic Renal Failure

A STUDY ABOUT THE CHANGES IN LEVELS OF
PANCREATIC ENZYMES IN CASES OF CHRONIC

RENAL FAILURE
DISSERTATION
Submitted to The Tamilnadu Dr.M.G.R Medical
University in partial fulfilment of the requirements for the
Degree of MD Biochemistry
Branch XIII
2011-2014
CERTIFICATE
Certified that the dissertation entitled “A STUDY ABOUT THE CHANGES IN
LEVELS OF PANCREATIC ENZYMES IN CASES OF CHRONIC RENAL
FAILURE” is a bonafide record of the work done by Dr.V.S. Deepa under our guidance
during her post graduate study during the period of 2011-2014 under THE TAMILNADU
Dr.M.G.R. MEDICAL UNIVERSITY, CHENNAI, in partial fulfillment for the degree of
MD in BIOCHEMISTRY, BRANCH XIII. It has not been submitted (partial or full) for the
award of any other degree or diploma.
Dr. S. Jaya, (Guide) Dr. J. K. Sathya Sudha Devi, (Co-Guide)

Professor, Professor & HOD,
Department of Biochemistry, Department of Biochemistry,
Sree Mookambika Institute of Medical Science, Sree Mookambika Institute of Medical Science,
Kulasekaram. Kulasekaram.
Kulasekaram. Kulasekaram
Kulasekaram
Department Of Biochemistry
Sree Mookambika Institute Of Medical Science
Kulasekaram
AKNOWLEDGEMENT
I bow to the almighty god, for showering upon me his blessings that gave me the courage
to venture out this thesis.
I extend my profound sense of gratitude to Dr. J.K. Sathya Sudha Devi, Professor and
Head of the Department of Biochemistry for her, direction, co-operation, constant
encouragement and immense patience with me at every step of this endeavour.
I am extremely thankful to my guide Dr.S.Jaya, Professor, Department of Biochemistry

for her valuable guidance & earnest support from the very beginning of the course.
I am very grateful to Dr.Velayuthan Nair, M.B.B.S, M.S. Chairman and

Dr.Rema.V.Nair, M.B.B.S, M.D, DGO Director, Sree Mookambika Institute of Medical
Science for providing the central lab facilities to accomplish my thesis work.
I am extremely thankful to Dr.Pethuru,MD, Assistant Professor, Department of

Community Medicine, Sree Mookambika Institute of Medical Science, Kulasekaram for
providing me with the timely statistical analysis involved in the study.
I take this opportunity to thank all the faculty members of the Department of Biochemistry,
Sree Mookambika Institute of Medical Science, Kulasekaram for the valuable support and
encouragement rendered by them.
With deep sense of gratitude, I remember the love, support, and encouragement I received
from my family for being with me throughout.
CONTENTS
Sl. No. Index Page No
1 List of Abbreviations
2 List of tables
3 List of graphs
4 List of colour plates
5 List of Appendices
6 Abstract
7 Introduction
8 Aims and Objectives
9 Review of literature
10 Materials and methods
11 Results and observations
12 Discussion
13 Summary and conclusion
14 Bibliography
LIST OF ABBREVIATIONS
CRF Chronic Renal Failure
GFR Glomerular Filtration Rate
ml/mt Milli litre / minute
ml/mt/m2 Milli litre per minute per metre square
CKD Chronic Kidney Disease
AFR Acute Renal failure
ESRD End Stage Renal Disease
AER Albumin excretion
EGFR Estimated Glomerular Filtration Rate
USA United States of America
% Percentage
GN Glomerulo Nephritis
DM Diabetes Mellitus
SLE Systemic Lupus Erythematosis
RF Renal Failure
MM Middle Molecule
BUN Blood Urea Nitrogen
CO2 Carbon di Oxide
G-6-P DH Glucose-6-Phosphate Dehydrogenase
RBC Red Blood Corpuscles
FSH Follicle Stimulating Hormone
LH Luteinizing Hormone
GH Growth Hormone
ECF Extra Cellular Fluid

GIT Gastro Intestinal Tract
mmol/lit Milli mole / liter
mmol Milli mole
PTH Parathyroid Hormone
CCK Cholecystokinin
S.amylase Serum Amylase
K.Da Kilo Dalton
RES Reticulo Endothelial System
U/L Units per liter
SU Somogyi Units
Hr Hour
ml Milli litre
CU Caraway Unit
Mg/dl Milligram per deciliter
ng/day Nanogram per day
Cam Amylase clearance
Ccr Creatinine clearance
Mg% Milligram percentage
mmol/L Millimole per litre
µL Microliter
IU/L International units per litre
CNP Chloro nitro phenol
nm Nanometer
ERCP Endoscopic Retrograde Cholangio Pancreatography

LIST OF TABLES
Table No. Title
Table 1 Comparison between mild and moderate renal failure
Table 2 Comparison between moderate and severe renal failure
Table 3 Comparison between mild and severe renal failure
Table 4 Correlation of serum amylase and serum urea in various study groups
Table 5 Correlation of serum lipase and serum urea in various study groups
Table 6 Correlation of serum amylase and serum creatinine in various study groups
Table 7 Correlation of serum lipase and serum creatinine in various study groups
Correlation of amylase clearance and serum creatinine in various study

Table 8
groups
𝐶𝑎𝑚
Table 9 Correlation of ratio and serum creatinine in various study groups
𝐶𝑐𝑟
Table 10 Correlation of serum calcium and serum creatinine in various study groups
Correlation of serum phosphorous and serum creatinine in various study

Table 11
groups
Table 12 Correlation of serum phosphorous and serum calcium in various study groups
LIST OF GRAPHS
Graph No. Title
Graph 1 Comparison of serum amylase in various study groups
Graph 2 Comparison of urinary amylase in various study groups
Graph 3 Comparison of Cam in various study groups

𝐶𝑎𝑚
Graph 4 Comparison of 𝐶𝑐𝑟
in various study groups
Graph 5 Comparison of serum lipase in various study groups
Graph 6 Comparison of serum calcium in various study groups
Graph 7 Comparison of serum phosphorous in various study groups

LIST OF COLOUR PLATES
Colour Title
Plate No
CP1 Collection of venous blood sample
CP2 Various blood collection tubes
CP3 Table top centrifuge
CP4 Seperation of serum
CP5 Semi auto analyzer
CP5 Structure of alpha amylase
CP6 Action of alpha amylase
CP7 Mechanism of action of lipase

LIST OF APPENDICES
Appendix No. Title
Appendix 1 Ethical Committee Certificate
Patient Information Sheet
English
Appendix 2
Tamil
Malayalam
Patient Consent Sheet
English
Appendix 3
Tamil
Malayalam
Appendix 4 Patient proforma

ABSTRACT
ABSTRACT
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INTRODUCTION
Introduction
CHRONIC RENAL FAILURE (CRF)
CRF is characterized by a progressive and generally irreversible decline CFR. Kidney
failure and be defined as either.
1. A level of GFR < 60 ml/mt/1.73 m2 for more than three months which is accompanied
in
most cases by signs and symptoms of uraemia (or)
2. Structural or functional abnormalities of the kidney with normal or decreased GFR in
the
beginning, but progresses to decreased GFR with time1.
CRF in caused by many diseases out of which glomerulonephritis the most important
cause.
Increase in the blood levels of non-protein nitrogenous substances is referred to as
azotemia which is the hallmark of Kidney failure. When azotemia is associated with signs
and symptoms of end stage renal failure it is termed as uraemic syndrome which is the
terminal manifestation of renal failure. It is characterized by failure of renal excretory
functions as well as metabolic and endocrine abnormalities.
It is also associated with electrolyte disturbances, anaemia,
atherosclerosis and hypertension leading to cardiovascular dysfunctions, poor immunity due
to leucocyte dysfunctions altered calcium metabolism leading to renal osteodystrophy,
gastrointestinal abnormalities causing anorexia, nausea, vomiting and even gastrointestinal
bleeding, neuromuscular abnormalities, myopathy and very rarely acute pancreatitis also.
Pancreatitis occurs with a high frequency in uraemic patients. Hemodialysis patients
are more likely to suffer from triglyceridemia which is a predisposing factor for pancreatitis.
Introduction
Diagnosis of these complications of CRF is also important as we can prevent the
further worsening of the condition of the CRF patient. Most of the complications of CRF can
be diagnosed based on clinical signs and symptoms. Some symptoms of CRF like abdomen
pain and vomiting can also be due to the development of acute pancreatitis in these patients.
Therefore pancreatic enzymes like amylase and lipase should be quantitated, which will show
a marked raise in their levels, when compared to the minimal raise of these enzymes in CRF,
if acute pancreatitis had complicated the CRF.
Even though acute pancreatitis is a complication of CRF, the incidence and
aetiopathology of acute pancreatitis complicating CRF is not known in our population. So the
present study was done to study the variations in pancreatic enzymes levels in CRF patients
without already known pancreatitis and also to determine the incidence of acute pancreatitis
in CRF patients.
AIMS AND OBJECTIVES
Aims and objectives
The main aim of the study is to investigate about the changes in levels of pancreatic
enzymes in cases of chronic renal failure.
The objectives of the study include the following:
a)To detect the incidence and prevalence of acute pancreatitis in known CRF patients
with or without dialysis.
b) To find out the diagnostic value of serum amylase by measuring the rate of
amylase clearance to the rate of creatinine clearance in relation to the stages of chronic renal
failure. (mild, moderate and severe).
C) To evaluate if serum creatinine, serum amylase and serum lipase have any
correlation with the severity of CRF(mild, moderate and severe)

REVIEW OF LITERATURE
Review of literature
THE KIDNEYS
Human Kidneys converts over 1700 litres of blood to about 1-1.5 litres of
concentrated fluid called urine per day. During this process, the Kidneys also serve to
excrete the waste products of metabolism, regulate the body’s water and salt, and maintain
appropriate acid base balance of plasma and serves as an endocrine organ secreting some
hormones like erythropoietin, calcitriol, renin and prostaglandins.
CHRONIC RENAL FAILURE
Chronic Kidney disease in explained as 1
i. Kidney damage for more than 3 months. It is defined by structural or functional
abnormalities of the Kidney with or without decrease in GFR and is manifested by
 Pathological abnormalities
 Markers of Kidney damage including abnormalities in the composition
of blood/urine/abnormalities in imaging tests.
ii. GFR less than 60ml/min/1.7m2 for more than 3 months with or without Kidney
damage.
Presence of CKD should be established based on the presence of Kidney damage and
the level of Kidney function (GFR) irrespective of the diagnosis. Based on the extent of
kidney injury kidney failure can be classified as follows.
Acute renal failure: A sudden loss of kidney function caused by an illness, an injury,
(ARF) or a toxin that stresses the kidneys (Kidney function may
recover)
Chronic Kidney Disease: A long and usually slow process were the kidney loses its ability
(CKD) to function
End-stage renal disease: When the kidneys have completely and permanently shut down
(ESRD)
BASED ON eGFR CHRONIC KIDNEY DISEASE IS STAGED AS;
Stage eGFR Description(Renal structure and function) Predominant
(mL/min/1.73 m2) AER status
1 ≥ 90 Kidney damage with normal/high GFR Micro
2 60-89 Kidney damage with mild reduction in GFR Micro
3 30-59 Kidney damage with moderate reduction in GFR Macro
4 15-29 Kidney damage with severe reduction in GFR Macro
5 <15 Kidney failure
AER = albumin excretion; eGFR = estimated glomerular filtration rate
PREVALENCE AND INCIDENCE OF CKD
Based on the data of National Health and Nutrition Examination Survey (NHANES)
reported in 2003, in the USA the estimated number of adults with CKD, staged 1, 2 and 3
was 10-11% of the total population.
The prevalence of CRF was predicted to be about 500 to 1000 patients per million
population2.
AETIOLOGY
The Kidney may be affected by a number of progressive diseases which can destroy
the nephrons and cause signs and symptoms of CRF. CRF is a syndrome which results from
progressive and irreversible destruction of nephrons regardless of the cause. In many patients
the condition progresses over a number of years and sometimes it is impossible to determine
the underlying renal disease.
The aetiological spectrum of CRF differs in different parts of the world.
Primary glomerulonephritis is the commonest cause of CRF in developing countries
of the world, whereas diabetic nephropathy is emerging as the most common cause of CRF in
developed countries where life expectancy of diabetes has increased considerably as a result
of better diabetic care3.
Diabetic and hypertensive nephropathy are the leading underlying aetiologies of both
CRF and ESRD4.
IMPORTANT CAUSES OF CRF
i. Primary Glomerulo Nephritis - Proliferative GN
- Focal glomerulosclerosis
- Membranous GN
- Membranoproliferative GN
- Crescentic
ii. Secondary glomerulopathy - Systemic diseases
(DM, SLE, Amyloidosis,

Vasculitis)
iii. Interstitial Renal diseases - Chronic Interstitial nephritis
- Chronic Pyelonephritis
- Reflux nephropathy
iv. Hypertensive Renal disease - Nephrosclerosis
- Renal artery stenosis
v. Obstructive nephropathy - Urinary Calculus disease
vi. Heredo familial renal disease - Autosomal dominant polycystic
Kidney Disease
- Medullary cystic disease
- Alport’s syndrome
PATHOPHYSIOLOGICAL CHANGES
1) Impairment in Concentration and dilution of urine
2) Impaired excretion and conservation of sodium.
3) Decreased excretion of Potassium with hyperkalemia is often the immediate life
threatening consideration in the management of patients with RF.
4) Excretion of acid.
5) Calcium, phosphate, vitamin D or bone homeostasis.
6) Impaired erythropoietin products leading to renal anaemia.
7) Impaired excretion of many substances and metabolites that act as uraemic toxins.
PROGRESSIVE NEPHRON LOSS AND ADAPTATIONS
In CRF the number of nephrons goes on decreasing with passage of time. As the
nephrons continue to be lost, the remaining undamaged or less severely damaged nephrons
undergo certain changes. Experimental studies have shown that single nephron GFR in the
remaining intact nephrons tends to increase and they undergo compensatory hypertrophy. At
this stage of the disease, GFR can be maintained normal despite the reduced number of
nephrons until the limits of increase of single nephron GFR is reached.
These beneficial compensatory adaptations in residual renal function ultimately have
harmful systemic and renal effects. These have been termed as trade off hypothesis5.
There is some evidence that supports the adaptive increase in phosphate excretion by
the nephron that typically occurs in CRF. It is thought to be mediated at least in part by
parathormone and the levels of this hormone have found to rise progressively throughout the
course of CRF. During the course of CRF, the hyperparathyroidism causes hyperplasia of the
parathyroid. The consequence of this secondary hyperparathyroidism however extends far
beyond the promotion of increased fractional phosphate excretion rates.
MIDDLE MOLECULE HYPOTHESIS (MM) 6
The discrepancy between the severity of symptoms and degree of azotemia seems to
be most marked in patients who are treated with maintenance peritoneal dialysis. Even
though the BUN and serum creatinine levels are high, the symptoms of uremia are mild and
peritoneal dialysis patients may be less prone to develop peripheral neuropathy than the
hemodialysis patients. Thus it is observed that the toxicity is related to the accumulation of
higher molecular weight substances which are cleared more readily by peritoneal dialysis
than by hemodialysis.
The peritoneal membrane is more permeable to solutes of middle molecular weight
(Approximately 500-3000 Daltons) when compared to hemodialysis membranes. According
to the middle molecule hypothesis, shortening the duration of dialysis will jeopardize the
removal of these compounds despite the same clearance of small solutes.
The MM hypothesis has a number of shortcomings. First the efficiency with which
dialysis corrects the uraemic syndrome argues in favor of low molecular weight solutes
playing the pathophysiological pre-eminent role. Second is that most solutes are of low
molecular weight and are not of MM size.
In summary the MM hypothesis remains controversial, despite a great deal of
research.
URAEMIC TOXINS7
Most of the manifestation of uraemic syndrome is due to the accumulation of toxic
products of normal or abnormal metabolism, most of them are products of protein and amino
acid metabolism.
Urea is the
nitrogen containing metabolic product of protein catabolism. It accounts for more than 75%
of non-protein nitrogenous substances excreted. An increase in plasma urea concentration is
known as uremic state. Some of the clinical abnormalities like anorexia, vomiting, malaise
and headache are contributed by urea itself. Urea exerts toxic effects in cells either directly
or indirectly when it is converted to ammonia and CO2, principally by bacterial urease.
Creatinine is the final product of phosphocreatine catabolism.
Measurement of its excretion rates are also used as indicators of kidney function. Serum
creatinine concentration is mostly used as an index of renal function.
Additional categories of nitrogenous excretory products include,
By products of proteins and amino acid metabolism:
-Guanidino compounds
-Guanidine
-Urates and hippurates
-End products of Nucleic acid metabolism
-Polyamines
-Phenols
-Benzoates
-Indoles
GUANIDINO COMPOUNDS
A Guandino compound as uremic toxins is still a controversy as it is difficult to
measure its plasma and tissue concentrations.
Guandino acetic acid, guanidine propionic acid and  - guanidine butyric acid can
cause auto hemolysis of RBC and inhibit G-6-P DH invitro.
In uraemic patients, plasma levels correlate inversely with erythrocyte glutathione
concentration, suggesting loss of protective effect of glutathione against hemolysis. Other
guanidine compounds may have neurotoxic effects.
Guanidine and MM have been related to peripheral neuropathy
while  -guanidino butyric acid, tauro cyanine, homoarginine and  -Keto -  -
guanidinovaleric acid may lower the seizure threshold.
ENDOCRINE DYSFUNCTION IN CRF6
Nature of Defect Hormonal defect
1. Diminished Production of Decreased erythropoietin
renal hormones production Decreased
conversion of 25-hydroxy
vitamin D3 to 125 – dihydroxy
vitamin D3
2. Hormonal hyper secretion Hyperparathyroidism and
to re-establish homeostasis secretion of natriuretic hormone
3. Decreased metabolic FSH, LH, Prolactin, GH etc
clearance of hormone
4. Defective tissue conversion Thyroxin to triiodothyronine, 25-
of prohormone to hormone hydroxy vitamin D3 to 125
dihydroxy vitamin D3
5. Decreased hormone Testosterone
production
6. End organ unresponsiveness Insulin, Parathyroid hormone
FLUID, ELECTROLYTE AND ACIDBASE DISORDERS DUE TO URAEMIA7
i. Sodium and water homeostasis
In most patients with stable CRF, the total body contents of sodium and water are
increased.
The underlying etiologic disease process may itself disrupt glomerulotubular balance
and promote sodium retention and ECF volume expansion. Such ECF volume expansion
contributes to hypertension, which in turn further accelerates progression of nephron injury.
When water intake exceeds the capacity of free water clearance, it leads to
hyponatraemia. Patients with CRF also have impaired renal mechanism for conserving
sodium and water.
ii. Potassium homeostasis7
In CRF the decline in GFR is associated with a proportionate decline in urinary
potassium excretion. Potassium excretion in the GIT is increased.

Hyperkalemia may be present in constipation, augmented dietary intake and protein
catabolism, hemolysis, hemorrhage, transfusion of stored RBC, Metabolic acidosis, following
consumption of certain medicines that inhibit potassium entry into the cells or potassium
secretion in distal nephrons.
Conditions like diabetic nephropathy and certain renal tubular acidosis are associated
with earlier and severe disruption of potassium secretary mechanism in distal nephrons.
Hypokalemia is uncommon in CRF and rarely occurs due to reduced dietary
potassium intake or excessive diuretic therapy or gastrointestinal loses.
METABOLIC ACIDOSIS
Advancing renal failure is associated with total urinary net daily acid excretion
limited to 30-40 m. mole and an anion gap of upto 20 m.mol/litre with a reciprocal fall in
plasma bicarbonate. In most patients, the metabolic acidosis is mild.
A LIST OF URAEMIC TOXINS 7, 8
 Creatine
 Creatinine
 Urates and hippurates
 End products of aliphatic amino acid metabolism
 End products of aromatic amino acid metabolism
 Tryptophan- Tyrosine- Phenylalanine
 Advanced glycation end products
 Inhibitors of ligand protein binding
 Glucurono conjugates and aglycones
 Inhibitors of somatomedin and insulin action.

 Review of literature
DIFFERENT PHASES OF CRF;
PHASE1-DECREASED RENAL RESERVE
In this phase the kidney function is almost normal. The basal GFR may be
normal or sometimes even elevated, but a rise in response to a protein challenge
which is expected is attenuated. Patient might not be symptomatic or have any
significant biochemical variations. Only creatinine clearance may change which is
lower than normal but above 50 ml/min.
PHASE 2-MODERATE RENAL INSUFFICIENCY
The Ccr is below 50 ml/min in this stage. The patient may usually present with
nocturia, decreased appetite and mild anemia.
PHASE 3-SEVERE RENAL INSUFFICIENCY
The Ccr at this stage is approximately 10- 15 ml/min. Serum creatinine rises to
5.5 to 7 mg/dl. This stage is symptomatic stage when anemia becomes severe
accompanied by metabolic acidosis, hypocalcemia, hyponatraemia and
hypochloremia.
PHASE 4-STAGE OF UREMIA
Now the renal function is only about 5-10 % of the normal. Serum creatinine
is more than 8 mg/dl. The patient is symptomatic with symptoms referred to all
organs. Hypocalcemia becomes frequent along with anemia, bleeding and bone
disease.
PHASE 5-END STAGE RENAL DISEASE
ESRD occurs when the fall in GFR is 5 to 10% of the normal, ie ≤3
ml/min. At this stage the patient requires renal replacement therapy.

SERUM AND URINARY CREATININE
These values are necessary in the study of amylase as the amylase clearance values
are compared with that of creatinine clearance. Reference ranges of serum creatinine are, 9
Serum or Plasma
Men : 0.8 – 1.3 mg/100ml
Women : 0.6 – 1.0 mg/100 ml.
Normal ranges of urine Creatinine is 0.5-2.0 ng/day10
Normal creatinine clearance is 95 – 105 ml/min.
(Creatinin e) Urine x volume of urine

Ccr =
(Creatinin e) serum x Time
PANCREAS
The pancreas is a flattened, elongated and soft organ which is oblique and is about 12
to 20 cm in length and lies behind the peritoneum of posterior abdominal wall.
PANCREATITIS
Acute pancreatitis can be defined clinically by a patient who presents with, -
Symptoms like epigastric pain, vomiting etc.
-An elevated serum amylase or serum lipase more than three times the upper normal
limit.
AETIOLOGY:
1) Obstructive causes:
-Gall stones (commonest)
-Stenosis of Sphincter of Oddi

-Ampullary/pancreatic tumors
-Parasites, clots or foreign bodies lodged in the ampulla
2) Toxic causes:
 -Alcohol
 -Drugs
 Immunosuppressants like azathioprine,6-mercaptopurine etc
 cyclosporine
 tacrolimus
 trimethoprim-sulfamethoxasole
 IV/aerosolized pentamidine
 antiviral drugs like 2,3-dideoxy inosine
 sulfasalazine
 oral 5-aminosalicylic acid
 tetracycline
 scorpion venom
3) Metabolic causes:
 hyperlipidemia
 hypercalcemia
4) Infectious causes:
 viral infections
 mumps
 coxsackie virus
 hepatitis B
 cytomegalovirus
 rubella
 HIV
 bacterial infections
 salmonella
 shigella
 hemorrhagic
 Escherichia coli
 Legionella
 Leptospira
 brucella
 parasitic infections
 ascaris lumbricoides can cause biliary pancreatitis
5) Autoimmune causes:
 sclerosing pancreatitis
 inflammatory bowel disease
 systemic autoimmune diseases
6) Genetic causes:
 mutation in cystic fibrosis transmembrane regulator
 mutation in trypsinogen gene
7) Iatrogenic causes:
 ERCP
coronary artery bypass
8) Neoplastic:
 primary pancreatic tumors
9) Vascular causes:
 ischaemia
 cholesterol emboli
 vasculitis
10) Other causes:
 trauma
 peptic ulcer
 childhood disease like sickle cell anemia
 annular pancreas
 duodenal diverticulum
 chronic renal failure
 food allergy
 ectopic pancreatic tissue
STAGES OF PANCREATITIS
Acute pancreatitis can be divided into two stages:
The first stage is the inflammatory stage which lasts for one week. During this
inflammatory stage the extent of severity of the disease is related to extra pancreatic organ
failure, which is considered as secondary effect of inflammatory response of the patient
which is triggered by acinar cell injury. During this first stage the patient has signs and
symptoms like fever, increased pulse rate, decreased blood pressure, leukocytosis and
respiratory distress. This is called Systemic Inflammatory Response Syndrome (SIRS).The
pathology involves multiple cytokines like PAF, TNF and interleukins. During this
inflammatory stage complications are rare. 75% to 80% of the patients recover at this stage
itself and only approximately 20%of the patients will enter the second stage of the disease.
The second stage of acute pancreatitis is more prolonged which may last from weeks
to months. Necrotization may also occur when the process is called necrotizing pancreatitis.
During this second stage the morbidity of the disease may be high due to organ failure,
infected necrosis etc. Patients suffering from second stage acute pancreatitis are also prone
for complications due to surgical intervention.
Acute pancreatitis can be classified according to the severity of the disease as follows:
(a) Mild- No peripancreatic complications and no organ failure.
(b) Moderate- Sterile peripancreatic complications or transient organ failure.
(c) Severe- Infectious peripancreatic complications or persistent organ failure.
(D) Critical- Infectious peripancreatic complications and persistent organ failure.
PATHOPHYSIOLOGY OF PANCREATITIS
The pathophysiology of acute pancreatitis involves the activation and release of
pancreatic enzymes in the interstitium which can cause auto digestion of the pancreas which
could be followed by multiple organ dysfunctions.
The basic changes which occur are:
a) Proteolytic destruction of the pancreas.
b) Necrosis of blood vessels.
c) Necrosis of fat.
All the above changes are accompanied by an inflammatory reaction. Interstitial
oedema is present in early stages. Later on frank necrosis of the endocrine and exocrine tissue
occurs.
The pancreatitis inducing substances blocks the secretion of zymogen granules from
the acinar cells which causes fusion of zymogen granules with the intracellular proenzyme
trypsinogen which forms intracellular trypsin and causes cellular auto digestion. The excess
trypsin generated exhausts the pancreatic secretory trypsin inhibitors inside the acinar cell
and the alpha-2-macroglobulin (nonspecific antiprotease) in the interstitium. Free trypsin also
activates other zymogen and also a cascade system of protease like the complement system,
coagulation, fibrinolysis and Kallikereum-kinin.
Trypsin also activates the complement system C5 which has a major role in
inflammatory cells formation. As the macrophages and neutrophils are more and more
stimulated, there is local spillage of arachidonic acid metabolites, clot promoting factors,
cytokines, platelet activating factors, Proteolytic and lipolytic enzymes. When all the above
factors exceed the scavenging capacity of antioxidant systems of the body, they interact with
the microcirculation of the pancreas resulting in thrombosis and hemorrhage.
Endothelial cell damage activates the local coagulation system by trypsin resulting in
interstitial oedema and leads to the formation of fibrin-platelet thrombus within the pancreatic
microcirculation.
Thus the activation of pancreatic enzymes lead to exacerbation of inflammation,
finally resulting in widening of regional necrosis.
COMPLICATIONS OF ACUTE PANCREATITIS
1) Myocardial depression is caused as acinar cells release myocardial depressant factor.

2) Acute Respiratory Distress Syndrome due to increased permeability of alveolar capillary
membrane. Pulmonary leucostasis and Proteolytic enzymes like elastase also trigger
ARDS.
3) Pleural effusion due to transfer of peripancreatic exudates through peridiaphramatic
lymphatic plexus.
4) Oliguria and renal failure result due to hypovolemia and deposition of fibrin in the
glomerular capillaries leading to acute tubular necrosis.
5) DIC due to photolytic effects of circulating trypsin.
As mentioned earlier there are many causes for acute pancreatitis. Even though it is
rare, chronic renal failure can also precipitate an attack of acute pancreatitis 11. Acute
pancreatitis can itself precipitate an attack of acute renal failure12. Acute renal failure
resulting from renal tubular necrosis is occasionally observed particularly in fulminant
pancreatitis13 which is due to fluid imbalance14.
Pancreatic disease may occur as one of the complications in renal failure patients,
although the exact incidence and pathogenesis of acute pancreatitis is not known15.
Acute pancreatitis in renal failure may be due to excess PTH, which would stimulate
calcium uptake by acinar cells. This altered calcium within the cell could lead to release of
the enzyme trypsinogen which is activated to trypsin within the pancreas causing lysis with
functional and histologic alterations16.Thus pancreatitis is initiated.
Increased gut hormones levels are found in renal failure patients. Cholecystokinin
(CCK) is also increased CCK can induce pancreatitis by causing increased secretion of
enzymes by the pancreas. It induces caspase activation and mitochondrial alterations in the
pancreatic acinar cells17.

Malignant hypertension, which is one of the complications of renal failure is also said
to precipitate pancreatitis. The pancreas is one of the organs most commonly affected with
the necrotizing lesions of malignant hypertension18.
It is possible that anatomical abnormalities of the pancreas like pancreatic ectasia,
interstitial inflammation and fibrosis, acinar ductal metaplasia, ductal or periductal
proliferation may make the patient with the end stage renal disease more susceptible to the
development of acute pancreatic disease when exposed to a variety of physiologic and non-
physiologic influences.
Several tests are used to evaluate the pancreatic exocrine function. Of this estimation
of pancreatic enzymes in body fluids is widely used as a screening test for acute pancreatitis.
Serum amylase, the most commonly estimated enzyme is found to be increased not only in
pancreatitis, but also in other conditions as the enzyme is also found in other organs in
addition to pancreas like salivary glands, liver, kidney, fallopian tubes etc.
Lipase determination exhibits good sensitivity and excellent specificity. Other
enzymes like trypsinogen19, elastase, and phospholipase A220 also have been found to be
elevated in acute pancreatitis. Trypsin and elastase remains elevated longer than that of S.
amylase.
Symptoms
Abdominal pain,
Nausea and vomiting
Serum Amylase Pancreatitis unlikely
Normal
Consider;Macroamylas
Serum Lipase emia, renal failure,
ischemic bowel,
Determine cause of parotitis, etc.
the pancreatitis
Evaluate pancreatitis
Severity
Fig 1. Evaluation of Pancreatitis
AMYLASE
Amylase is an important starch splitting enzyme which is increased in pancreas
abnormalities. In 1916, stock found that amylase activity in blood and urine was a sensitive
and reliable test for various pancreatic disorders21.
HISTORY
The term amylase is coined from the Greek word “Amylon” which means starch
splitting, originally it was named diastase by Payen and Persoz when they precipitated it from
Malt22.
Diastase was derived from the word diastasis meaning separation. Megendic found
amylase in the year 1846 and Foster measured it quantitatively in animals23.
DEFINITION
Alpha amylase is an enzyme that acts on starch, glycogen and other polysaccharides24.
It acts in a random fashion splitting the alpha-1,4- glucosidic bonds of a polysaccharide.
Pancreatic and salivary amylases are alpha amylases, while beta amylases are of plant origin
(Alpha 1, 4, glucon maltohydrolase).
CHEMISTRY
Amylase has molecular weight of 55.4 K.Da and acts at an optimum pH of 7.0. It
requires Calcium and chloride for optimum enzyme activity.
AMYLASE ISOENZYMES
Amylase activity can be detected in many tissues. Therefore the presence of amylase
in a tissue does not necessarily imply that it is the source of the enzyme. Contributions from
several organs are responsible for the serum amylase and the diseases that involve tissues and
viscera other than pancreas can also cause S1 amylase elevations.
Berk and his coworkers discovered that discrepancies in the findings were dependent
upon the method used. On the basis of polyacrylamide gel electrophoresis, Sephadex
chromatography and Isoelectrical focusing, it is believed that serum and urinary amylases can
be fractioned into two principle isoenzymes25, 26. The first is pancreatic type (P – Type) and
the second salivary type (S-Type) which chromatographically resembles the amylase derived
from organ extracts of pancreas and salivary glands respectively. Each isoenzyme may be
composed of slightly different subunits as evidenced by chromatographic mobility27, 28.
Many evidences obtained from normal subject, pancreatectamized dogs and
individuals with acute pancreatitis suggest that p- type isoamylase in serum and urine is
derived from pancreas29.
S-type is not only from the salivary glands but also from other organs30. In normal
serum the S-type component may be from other organs like fallopian tubes, ovaries, lungs,
prostate and liver31, 32.
Another type of isoamylase described was X type which may be probably derived
from S-type isoamylase. This isoamylase was found in normal urine, in sera of cancer lung
patients and also in human milk33.
In a normal person, the total serum amylase activity results from both pancreatic and
salivary type isoamylases, the pancreatic type was nearly 50% of the total isoamylase
activity34.
The two major isoenzymes are similar to each other except a slight variation in aminoacid
composition35. The diversity of isoenzymes observed within the pancreatic and salivary
isoamylase are due to occurance of several genetic alleles. Multiple species with each allelic
family are then formed by post translational modification35 such as glycosylation,
deglycosylation and deamidation. Many minor isoenzyme forms found by electrophoresis
are believed to be the result of post translational deamidation. In addition, some patients
demonstrate abnormally migrating isoamylases that contain sialic acid residues which are not
normally present in human amylase isoenzymes. Three to six minor P-isoamylases (P1 – P6)
and four to five minor S-isoamylases (S1 – S5) are known. The normal pattern that is usually
seen is P2 S236.
P3 minor isoamylase is seen in acute pancreatitis and in renal failure37.It is considered
as a more specific marker of acute pancreatitis than serum amylase alone.Hyperamylasemia
is associated with an increase in P3 isoamylase only when pancreatitis is present38.
METABOLISM
From the metabolism of P and S-type isoamylases in Baboon, an animal in which the
serum level and renal clearance of amylase are similar to those of man39. Duanne et al has
found out that40:
1. Most of the amylase was cleared by an external mechanism probably by the Reticulo
Endothelial System (RES) and only around 24% of amylase is cleared by urinary
excretion.
2. As the half-lives of these enzymes are approximately 130 minutes the metabolic
clearance of this enzyme is rapid.

3. Renal clearance of pancreatic isoamylase is almost 80% more rapid than the clearance
of salivary isoamylase.
Renal excretion of amylase takes place by glomerular filtration and tubular
reabsorption41, 42.
Serum amylase is regarded as the single most important practical diagnostic test in
acute pancreatitis. A raise in the level of serum amylase at least three times that of upper
normal limit favors the diagnosis of acute pancreatitis.
Serum amylase rises within 12 hours after the onset of acute pancreatitis and becomes
43
normal within 3to 5 days . The rise may be due to Trans peritoneal absorption of the
enzyme44, 45
and other factors like changes in the metabolism and renal secretion. Serum
amylase levels return to normal levels within 3 to 5 days usually46. Sometimes normalization
occurs rapidly indicating early resolution of the disease or extensive pancreatic necrosis or
acute exacerbation of chronic pancreatitis46, 47.
Also when pancreatitis is associated with triglyceridemia serum amylase
determination may be spuriously normal. Persistant hyperamylasemia if present suggests
ongoing inflammation or complications such as pancreatic pseudocyst or abscess48, 49.
Now it has been found that urinary amylase estimation in acute pancreatitis is more
diagnostic of the disease than serum amylase as it rises relatively earlier and higher and
persists longer50. Contrary to a normal individual who does not show any variation in urinary
amylase output within 24 hours period51 wide fluctuation in the rate of urinary amylase
excretion is seen in acute pancreatitis in a short period of time or within two hours which did
not bear any relation to the clinical condition of the patient51. Hence when one hour urine
amylase may be raised intermittently, the 24 hours urine amylase may be normal, so a raised
24 hour urinary amylase is significant but is misleading if normal and to be accurate in cases
of acute pancreatitis one hour urinary amylase determination every 8 to 12 hours is preferred
which is more practical and gives fewer false negative data.
Urinary amylase excretion is more sensitive index of acute pancreatitis52.This is due
to a temporary disruption of reabsorption of amylase by the tubules. This is believed to be
produced by the toxic substances which are released from the inflamed pancreas.
When serum levels are increased marginally or where amylase values have to be
correlated with clinical findings, it will be advantageous, if amylase clearance values are
studied. In an attempt to do this, Levitt et al studied in detail the amylase clearance and other
related values53.
CLEARANCE OF AMYLASE (Cam)
After knowing the serum and urinary amylase values, the rate of amylase clearance
(Cam) can be calculated as it also helps in the diagnosis of various diseases elaborated. To
calculate the Cam, the following formula can be used.
amylase (Urine) x volume of urine

Cam =
Amylase (serum) x Time
According to Michael D. Levitt, the average normal cam is 2-9 ml/minute which is increased
in pancreatitis.
Cam / Ccr Ratio
This ratio can be obtained directly from the amylase and creatinine clearance values
but in those cases where timed urine collection is not possible the ratio can be obtained from
the following formula.

Cam (Amylase) Urine x (Creatinin e) Serum

% x100
Ccr (Amylase) serum x (Creatinin e) Urine
According to Levitt et al Normal Cam/Ccr ratio is 2.30.097 (Range 1-5%)
In acute pancreatitis the Kidney clears amylase at a markedly increased rate due to
which Cam/Ccr is increased54, which persists even after the serum amylase returns to normal,
because urinary amylase takes a longer time to return to normal. So this ratio is said to be a
Cam
sensitive indicator of pancreatitis55. The cause of increased ratio is due to transient
Ccr
reduction in renal tubular reabsorption of amylase56. The nature of the tubular defect is not
yet fully clarified; however renal tubular dysfunction may not be the only explanation for this
increased clearance. Renal tubular dysfunction may reflect transient inhibition by a
pancreatic enzyme or toxins or possibly interference with normal tubular reabsorption of
amylase by the presence of other low molecular weight proteins that are released in acute
pancreatitis as well as in other catabolic illness57.
Cam/Ccr ratio is also increased in diabetic Ketoacidosis54. Among the possibilities
that have been postulated are hyperglucagonemia causing renal excretion of amylase, an
increased amount of low molecular weight proteins competing with amylase for renal tubular
absorption increases the S- type rather than P–type isoamylase and interference by Ketone
bodies with the measurement of serum creatinine in diabetic ketoacidosis.
NORMAL VALUES AND THEIR MODE OF EXPRESSION
P iso-enzyme in new born is around only 3% of adult range. The serum activity
increases with age and reaches the adult range at around 8 months of age58. The S isoamylase
in newborn is around 32% of adult range. It begins to increase by 3 – 4 months of age and
reaches adult levels (about 80 U/L) at around 5 Years of age59.
The normal values of serum and urinary amylase according to various methods of
estimation are as follows:
SOMOGYI METHOD
A Somogyi Unit is defined as a unit that is a measure of the hydrolyzing action of
serum amylase on starch and that is equivalent to the amount of enzyme in 100 milliliters of
blood serum required to produce 1 milligram of glucose when acting on a standard starch
solution under defined conditions.
The values of serum and urinary amylase by this method are expressed in
Somogyi Units (SU) per 100 ml. The normal values are:
Serum amylase: 60 – 160 SU/100 ml
Urinary amylase: 35 – 260 SU/ hr60, 61
CARAWAY METHOD
In this method the serum amylase value is expressed in Caraway Units (CU) per 100
ml. The caraway unit is approximately equal to Somogyi Unit. The normal value of serum
amylase is 9532 CU/100 ml62.

HUGGIN AND RUSSEL METHOD63
In this method serum amylase is expressed in units / 100 ml. Normal value of serum
amylase is 9 – 35 U.
HENRY AND CHIAMORI METHOD64
In this method serum amylase values are expressed in units/100ml. The normal
values are
Serum amylase is males : 38 to 118 U/100ml
Serum amylase in females : 46 to 141 U/100 ml
On the whole serum amylase in adults is 40 – 140 U/100 ml
Urinary amylase: 66 – 870 units / 100 ml or 43 – 245 Units / 24hrs.
AMYLOCHROME PROCEDURE65
According to this procedure
Serum amylase: 45 to 200 AMYLOCHROME UNITS / 100 ml
Urinary amylase: 40 to 330 AMYLOCHROME UNITS / hour

ENZYME COUPLED METHOD
Serum amylase-5 to 21 IU/L.
HYPERAMYLASEMIA AND HYPERAMYLASURIA
Any increase in the serum or urine amylase from the above mentioned normal value is
known as hyperamylasemia and hyperamylasuria respectively. This may be due to :
1. Pancreatic disease
2. Non Pancreatic diseases
3. Salivary gland disorders and
4. Disorders of other complex origin.
I. PANCREATIC DISEASES
A. Pancreatitis
1) Common causes
 Alcoholism
 Gall bladder disease
2) Uncommon causes
 Vasculitis
 Uraemia
3. Drug induced
(eg) Chlorthalidone
Tetracycline
Thiazide diuretics
Oral contraceptive steroids
4. Post endoscopy
5. Post-operative
6. Renal transplantation
B. Pancreatic carcinoma
C. Pancreatic trauma
II. NON PANCREATIC DISEASES
1. Renal insufficiency
2. Tumor hyperamylasemia
III. SALIVARY GLAND DISORDERS
1. Mumps
2. Calculi
3. Sialadenitis
4. Maxillofacial surgery
5. Drugs – Oxyphen butazone, phenyl butazone
6. Parotitis
7. Trauma
IV. DISORDERS OF OTHER COMPLEX ORIGIN
1. Biliary tract disease
2. Intra-abdominal causes other than pancreatitis.
a. Perforated gastric ulcer
b. Intestinal obstruction
c. Ruptured ectopic pregnancy
d. Mesentric infarction
e. Afferent loop syndromes
f. Aortic aneurysm with dissection.
g. Peritonitis
h. Acute appendicitis
i. Salphingitis
3. Cerebral trauma
4. Burns and traumatic shock
5. Post-operative hyperamylasemia
6. Diabetic ketoacidosis
7. Renal transplantation
8. Pneumonia
9. Acquired Bis albuminemia
10. Prostatic disease
11. Drugs – anticoagulants, salicylates, corticosteroids.
12. Pancreatic pleural effusion.
13. Mediastinal pseudocyst
14. Pregnancy
15. Review of literature
EVALUATION OF PANCREATITIS
Pancreatic amylasemia
With or without
lipasemia
Symptoms No symptoms
Pancreatic Previous pancreatitis Occasional

Aspecific or other pancreatitis finding
diseases
Illness Illness Familial Drugs

Difficult Post-Surgery
discharge of Post-ERCP
pancreatic juice Dyslipidemia
Pancreatitis Macroenzymemia
Abdominal or Viral hepatitis
(Acute, systematic
recurrent, Systemic diseases
diseases SO Malignancy
chronic
dysfunction,
Wirsung’s duct
stenosis
LIPASE
Lipase is also one of the pancreatic enzymes which are elevated in pancreatitis.
Lipase is the enzyme that catalyzes the hydrolysis of lipids.
Serum lipase is more specific and sensitive indicator to diagnose acute pancreatitis as
the serum lipase is mostly of pancreatic origin66, 67.
Serum lipase increases in the serum usually on the first day of clinical illness like that
of amylase68, 69. It also remains elevated for a longer period of about 10 days70, 71.
Many lipases are found in Gastro intestinal tract like lingual lipase, gastric lipase,
pancreatic lipase, phospholipase A2 and pancreatic nonspecific lipase. Apart from this
adipose tissue also contains lipoprotein lipase, liver contains hepatic lipase and endothelium
synthesizes endothelial lipase72. But the extent to which these nonpancreatic lipases
contribute to serum lipase levels has not been elucidated.
Phospholipase A2 splits the fatty acid of lecithin to form lysolecithin.
This lysolecithin damages the cell membrane. In acute pancreatitis phospholipase A2 is
activated in the pancreatic duct to form lyolecithin which can disrupt the pancreatic tissue and
also necrotize the surrounding fat.
Pancreas is the major source of serum lipase whose molecular weight is

73
approximately 50,000 . It occurs in several molecular forms. Although a more exact
description of the isoenzymes are needed, at least 2 forms are known to exist that differ in
molecular size, ionic strength requirements, co-lipase requirements, thermal stabilities etc74.
As their molecular properties are better characterized, the usefulness of measuring the lipase
associated with acute pancreatitis may improve75.
MECHANISM OF ACTION
Lipase hydrolyzes emulsified triglycerides of long chain fatty acids76. The site of
action of lipase is the interface between the oil drops and the aqueous phase77, so that the
degree of emulsification plays an important part in establishing the active substrate
concentration.
This distinguishes lipase from esterase which reacts with water soluble substrates. Pancreatic
lipase acts in the presence of colipase and bileacids78 at a pH range of 6 – 8, with a rapid fall
in activity below pH 579.
Lipase preferentially hydrolyses the outer 1 and 3 fatty acids. Its action on 2-
monoglyceride is weak and is probably advantageous in providing a mechanism for the
entry of glycerol into the cell, where it is required for re-esterification.
CH2 O C R1
CH2 OH R1 COOH
O
Lipase CH OH + COOH
CH2 O C R2 + 3H2O R2
O CH2 OH R3 COOH
CH2 O C R3
Glycerol Fatty Acid
O
Tri Acyl Glycerol
RENAL HANDLING OF PANCREATIC LIPASE
As lipase is completely absorbed by the proximal convoluted tubules after filtration
by the glomerulus, lipase is not found in urine of healthy people80. Therefore there is no
lipolytic activity in urine.

NORMAL VALUES OF SERUM LIPASE
Cherry and Crandall unit: 0.01 to 1 conventional unit. One conventional unit represent
50 micro mole of fatty acid split off in 180 minutes reaction run or 500/180 = 0.2778
micromole per minute.
The conditions in which there is hyperlipasemia81,82 :
1. Acute pancreatitis
2. Renal insufficiency
3. Dyslipidemia
4. Hyperlipidemia
5. Hepatobiliary disorders
6. Other intra-abdominal conditions like Irritable bowel syndrome
In acute pancreatitis, the serum lipase values increase like that of amylase because of
its absorption into general circulation from pancreatic bed. Even when the serum amylase
level has reached normal, the serum lipase in acute pancreatitis is one of the valuable aids to
the diagnosis of the same.
Serum amylase level is increased in many other conditions. The
estimation of serum lipase in those conditions will exclude the diagnosis of pancreatitis in
those cases. But in abdominal conditions the serum lipase levels are also increased making
the diagnosis difficult.
Patients with hypertriglyceridemia are prone to develop acute pancreatitis. This is because the
lipase in the pancreatic capillaries hydrolyze the triglycerides to release free fatty acids. This
in turn activates the trypsinogen to cause pancreatic capillary damage. In such cases even if
the serum amylase is normal , hyperlipasemia will be present83.
SERUM CALCIUM IN PANCREATITIS
Most of the patients with pancreatitis have hypocalcaemia. This may be due to
hypoalbuminemia which accompanies acute pancreatitis or sometimes patients suffering
from pancreatitis also have decreased free calcium ion irrespective of hypoalbuminemia.
If this type of hypocalcaemia occurs the prognosis is poor.
SERUM CALCIUM AND PHOSPHORUS IN CRF
Impaired kidney function is associated with variations in electrolytes
concentration. This may be due to bone disorders which occur in CRF. The main
pathophysiological changes which occur in bone disorders are increased PTH which leads to
abnormal mineral metabolism. CRF leads to decreased phosphate excretion causing hyper
phosphatemia. Increased levels of phosphorus in the blood acts on the 1-hydroxylase enzyme
and decreases its activity leading to decreased synthesis of 1, 25-Dihydroxy
cholecalciferol/calcitriol , which is the active form of vitamin D.
When the synthesis of calcitriol is decreased, the calcium absorption from the
gastro intestinal tract is also decreased. This causes hypocalcaemia. Thus hyperphosphatemia
can cause hypocalcaemia by decreased synthesis of calcitriol.
Hypocalcaemia and hyperphosphatemia together leads to increased synthesis
of PTH and increased proliferation of parathyroid cells, which ultimately leads to secondary
hyper parathyroidism.
Thus increased PTH stimulates the osteoblasts of the bone to cause a high bone
turnover. Low bone turnover diseases occur in osteomalacia. Disorders which occur due to
decreased bone turnover are accompanied with decreased number of osteoclasts and
osteoblasts and reduced activity of osteoblasts also.
Demineralized bone matrix is seen in osteomalacia. Therefore serum levels of
calcium and phosphorus should be estimated in the early stages of CRF to assess the
electrolyte and bone metabolism.
LABORATORY FINDINGS IN ACUTE PANCREATITIS
1. Pancreatic Enzymes in Body Fluids
Serum amylase : Elevated particularly P – isoamylase
Urinary amylase : Elevated
Cam / Ccr % : Elevated
Serum lipase : Increased
Pleural and Peritoneal fluid : Elevated amylase levels are found
Other Enzymes : Trypsin, phospholipase A2, elastase are
found to beelevated in acute pancreatitis.
Methaemoglobin : Increased
Serum triglycerides : Increased
2. STANDARD BLOOD TESTS
Increase in serum bilirubin, alkaline phosphatase and aspartate transaminase is more
in biliary tract disease than in alcoholic pancreatitis.

Blood glucose – Elevated because of increased glucagon.
Serum calcium – Lowered because of loss of albumin into the retroperitoneum,
partially because of calcium soap formation and possibly because of effects of paratharmone.
In case of acute renal failure occurring as a complication, blood urea nitrogen and
serum creatinine may be elevated.
Circulatory may be elevated failure leading to lactic acidosis and hence increased
lactate Dehydrogenase.
3. Tests for Anatomic Derangement
X-ray, ultrasonography, CT scan
As mentioned earlier, P2, S2 Pattern is normally seen,
when serum is electrophoresed. In acute pancreatitis, the P – type isoamylase is more than S
– type. Even when the serum amylase reaches normal in acute pancreatitis, the serum does
contain an elevated level of P-type isoamylase. In acute pancreatitis, the isoenzymes pattern
is P2, P3, S2, P3 which is normally undetectable in normal serum81. The origin of P3 in acute
pancreatitis remains unclear. A comparison with acquired Bis albuminemia may provide a
possible explanation of its origin. In acquired Bis albuminemia, electrophoresis of serum
proteins show a double band for albumin, one is corresponding to the normal albumin, the
other an abnormal band migrating more anodally. The latter is thought to be a product of
hydrolysis of normal albumin by pancreatic peptidase. Such a process may involve some
pancreatic proteins and P2 isoamylase be hydrolyzed by this process to give the faster enzyme
P3.Post translational modifications (deamidation or deglycosidation) were described by

Merritt and Karn84, 85. Such modifications of P2 induced by pancreatitis could also account
for P3. Evaluation of the Kinetics of P3 concentration in sera shows a peak of P3 appearing
latter than that of P2. The delay of the peak value of P3 is possibly explained by the time
required for it to be produced from P2.
ACUTE PANCREATITIS IN RENAL FAILURE
Serum amylase, P-isoamylase and lipase levels are increased in renal failure patients
both in chronic and also in acute renal failure86, 87.
THE REASON FOR INCREASED AMYLASE IN RENAL FAILURE
Renal Failure
1. Only approximately 24% of amylase is handled by the kidney88.
2. P- isoamylase is filtered 80% faster than salivary isoamylase.
Because of reduced renal function, the P – isoamylase is not filtered by the Kidney.
Hence P – isoamylase and total amylase levels increase in renal failure patients.
Even though the total amylase is elevated in renal failure patients, it is never more
than 2 fold. This is because only 24% is handled by the kidney and the rest of the amylase is
handled by the reticuloendothelial system89.
The interpretation of hyperamylasemia in CRF patients with pain abdomen becomes
difficult. The renal clearance ratio for amylase and creatinine has been suggested as a useful
aid in such a situation.

Previous reports have stated that the ratio of amylase clearance to creatinine clearance
remains normal in renal insufficiency and is increased in the presence of pancreatitis 53, 90.
But it has been proved that even in renal failure patients the Cam / Ccr ratio is elevated91, 92.
The increase in serum amylase is less than corresponding rise in serum creatinine. The
increased Cam / Ccr ratio must also be related to greater rise in serum creatinine than in
serum amylase. A decrease in the renal function does not reduce amylase clearance and
creatinine clearance proportionately. In severe renal failure, the Ccr is reduced out of
proportion to Cam thereby increasing the ratio93.
As mentioned above the presence of significant P3 activity has been associated almost
exclusively with acute or chronic pancreatitis, with pancreatic pseudocyst and sometimes
with renal failure because of decreased clearance of the enzyme. When P3 is detected in renal
failure, without clinical pancreatitis, diagnosis confusion can be reportedly minimized by
measuring the fractional percentage of the pancreatic isoamylase. As explanation, it has been
suggested that impaired renal excretion of plasma amylase facilitates post-translational
modification of the pancreatic P2 form within the circulation with the formation of the P3
isofoms94.
SERUM LIPASE IN RENAL FAILURE
Even though this also is one of the diagnostic aids in acute pancreatitis, this has been
proved to be elevated in renal failure patients95, 96.
THE REASON FOR ELEVATED LIPASE LEVELS
Lipase is removed from the serum mainly by glomerular filtration. Reabsorption of

lipase is almost complete in contrast to that of amylase97. The difference in handling of both
enzymes is due to their differing affinities for hydrophobic and hydrophilic surfaces. Serum
lipase activity appears to increase proportionately to the degree of renal failure, up to a
maximum of approximately 4 times of normal value87,98.
The patients with end stage renal disease and who were on maintenance hemodialysis
also have elevated serum amylase, P-isoamylase and serum lipase values. There is no
significant difference in pancreatic enzymes between pre and post hemodialysis sample99.
MATERIALS AND METHODS
Materials and methods
The present study was carried out at the Nephrology unit of Sree Mookambika
Institute of Medical Sciences, Kulasekaram from August 2012 to May 2013 for a time period
of 10 months. This cross sectional study was approved by the institutional Human Ethical
Committee. Voluntary informed consent was taken from all the subjects of the study.
SOURCE OF DATA
Fifty patients suffering from Chronic Renal Failure were selected from the
Nephrology ward as well as Nephrology outpatient department of Sree Mookambika Institute
of Medical Sciences, Kulasekaram. The history of the patient was taken by audit
questionnaire.
STUDY GROUP
Based on the serum urea and serum creatinine values the CRF patients were categorized in to
three groups for the study
GROUP 1: Mild CRF (Serum Urea 40-80 mg% and serum creatinine 0 to 3mg %)
GROUP 2: Moderate CRF (Serum Urea 81-100 mg% and serum creatinine 3.1 to 4.5 mg %)
GROUP 3: Severe CRF (Serum Urea >100 mg% and serum creatinine 4.6 to 8 mg %)
TYPE OF STUDY: Cross-Sectional Study
INCLUSION CRITERIA
Fifty patients with CRF from Nephrology Department of Sree Mookambika Institute
of Medical Sciences between the age group from thirty to eighty years were included in the
study.
EXCLUSION CRITERIA
1) Chronic alcoholics with portal hypertension.
2) Known case of previous pancreatitis

Parameters to be studied
Serum Urea, Serum Creatinine, Serum Amylase, Serum Lipase, Serum Calcium,
Serum Phosphorus, Uninary Amylase and Urinary Creatinine.
Sample collection
In the diseased patients studied, a sample of timed 4 hours urine was collected in
sterile containers during which period about 5 ml blood was collected in a red capped
Vaccutainer. Blood samples were then centrifuged at 3000 rpm for 10 minutes and the serum
was separated for further tests.
ESTIMATION OF SERUM AMYLASE
METHOD (CNPG3 Kinetic Method)
Historically various methods have been used, but all have relied on either an ill-
defined substrate (starch) or the use of helper enzymes with defined substrates. Here we
describe the direct colorimetric assay for  – amylase in which a defined substrate is used
that is predominantly cleaved directly by  – amylase to yield free chromophore. The
reaction is α Amylase
5CNPG3 3CNP + 2 CNPG3 + 2 Glucose + 3 Maltotriose
Rate of increase in absorbance due to formation of CNP is measured at 405 nm and is
proportional to the  -amylase activity in the sample.

REAGENTS
Amylase Mono Reagent (R1)
R1 MES buffer pH 6.0 90 mmol/L
Sodium Chloride 500 mmol/L
Pottasium Sulpha cyanide 0.60 mol/L
Calcium Acetate 7.2 mmol/L
CNPG3 2.7 mmol/L
PREPARATION OF THE REAGENT:
Peracetylation of maltotriose with acetic anhydride was done in the presence of
sodium acetate which acts as catalyst ,at 120 to 140 degree centigradefor 1 to 2 hours. This
results in formation of a peracetate with beta configuration at the anomeric carbon. This is
then heated with 3 to 10 equivalents of phosphorus pentachloride along with carbon tetra
chloride or chloroform (supporting solvent).This results in formation of a melt which is then
further heated at 70 to 90 degree centigrade for 3 to 8 hours to give 1-beta-chloro-2-trichloro
acetyl derivative which is then de-trichloro acetylated to 1- beta-chloro-2-hydroxy derivative
by treating with saturated ammonia in diethyl ether for 10 to 60 minutes at 0 to 10 degree
centigrade. This is then treated with a secondary amine in an aromatic hydrocarbon like
benzene or toluene at 15 to 30 degree centigrade for 8 to 24 hours which results in formation

of an alpha-anhydride. This anhydride reacts specifically with the hydroxyl group of the
chromogen in an aromatic solvent like toluene to yield alpha-maltotriosides. Equimolar
concentration of chromogen and the anhydride are mixed and refluxed for 4 to 24 hours in
toluene or benzene. When the alpha maltotrioside is deacetylated, a less side product is
formed which is usually associated with the reactions at the glycosidic bond. The compound
is reacted with a mixture of concentrated hydro chloric acid, methanol and chloroform in the
ratio 1:10:4 respectively at 20 to 25 degree centigrade for 2 to 4 days to give deacetylated
alpha-maltotriosides which was then isolated by neutralizing the acid, removing the residual
organic solvents and freeze drying.
Specimen
Unhemolysed serum should be used EDTA or citrate should not be used as
anticoagulant as they decrease the activity of the enzyme by 15%.
Procedure
The semiautoanlyzer was programmed as per the assay parameters.
BLANK SAMPLE
Working reagent 1000µl 1000µl
Distilled water 25 µl -
Sample - 25 µl
1000  L of the reagent and 25  L of serum was taken in a test tube and mixed well.
Reading was taken in the semi auto analyzer.
LINEARITY
The reaction is linear up to a concentration of 1000 units per litre. Samples with values more
than 1000 U/L must be diluted with normal saline.
Reference Range
Serum  -amylase activity is 35– 115 IU/L.
ESTIMATION OF URINARY AMYLASE
The procedure is the same except that the sample was diluted with purified water in
the ratio 1:5. Instead of serum, diluted urine was added and all the steps were followed as for
serum amylase determination.
Reference range
Urinary  -amylase activity is up to 1360 IU/24 hours.
ESTIMATION OF SERUM LIPASE
Ready to use two liquid reagent systems was used.
Principle
The Chromogenic lipase substrate 1,2-0- dilauryl – rac – glycerol -3-glutaric acid
ester (6 – methyl resorufin) is cleaved by catalytic activity of lipase to form 1,2-0- dilauryl –
rac – glycerol and an unstable intermediate glutaric acid ester. This decomposes
spontaneously in alkaline medium to form glutarate and methyl resorufin. The lipase activity
in the serum is proportional to the rate of formation of methyl resorufin and can be
determined photo metrically at 578 nm.
1,2, - O-Dilauryl – rac – glycerol – 3 – glutaric acid – ester

(6 methyl resorufin)
Lipase / Colipase
1,2, - O-Dilauryl – rac – glycerol +glutaric acid

(6 methyl resorufin) ester
Lipase / Colipase
Alkaline medium
glutaric acid + methyl resorufin
COMPONENTS
Reagents Concentration
R1 Bicin buffer (pH 8) 50 mmol/lt
Colipase  1 mg/lt
Sodium deoxycholate 1.6 mmol/lt
Calcium chloride 10 mmol/lt
R2 Tartarate buffer (PH4) 10 mmol /lt
Tauro deoxy cholate 8.8 mmol/lt
1,2 – o-Dilaury – rac – Glycero – 3 glutaric 0.27 mmol/lt
acid – 6 Methyl / resorufin

Specimen Collection
Serum is preferred. Lipase activity in serum is stable for 5 days at 2-8oC or for 24
hours at 20-25oC.
Procedure
Reagent blank Calibrator Serum/Plasma
R1 0.8 ml 0.8 ml 0.8 ml
Distilled H2O 0.01 ml 0.08 ml 0.8 ml
Mix and incubate for five minutes at 37o C
R2 0.2 ml 0.2 ml 0.2 ml
800  l of R1 and 200 of R2 was taken and mixed well. It was incubated at room
temperature for 5 minutes. Then 10  l serum was added and mixed well. Then the value
was read in the Semi atuto analyzer.
Reference Interval
Serum lipase activity is 13-60 IU/L
If lipase activity exceeds 300 IU/L, dilute the specimen with normal saline and repeat
the assay. That result should be multiplied with dilution factor to obtain the correct lipase
activity.
Estimation of serum urea
Serum urea was determined by kinetic UV method using Gesan kit.
Principle
Urea is hydrolysed in the presence of water in urease to produce Co2. The ammonia
formed in the first reaction combines with  - Ketoglutarate and NADH which in the
presence of glutamate dehydrogenase form glutamate and NAD+. The decrease in
absorbance at 340 nm due to depletion of NADH is proportional to the urea concentration in
the sample
Reagents
Concentration
R1: Goods buffer pH 7.6 130 mmol/l
ADP 1.2 mmol/l
Urease  8000 u/l
GLDH  1500 u/l

R2 Goods buffer pH 10.2 100 mmol /l
 - ketoglutarate 65 mmol/l
NADH 1.2 mmol/l
Reagents are liquid and ready to use. About using as mono reagent pour the content of R2
vial into the R1 vial and let stand for 6.15 minutes at least. For minority use add 1 ml of R2
reagent to every 4 ml of R1 reagent. Keep the reagents out of the refrigerator only for
use.
Store the kit at 2-8oc. After opening the vials, R1 and R2 are stable for 90 days if
recapped, immediately and is protected from contamination, evaporation, direct light and is
stored at the appropriate temperature. The working solution (R1+R2) is stable for 20 days at
2-8oC.
Specimen collection
Specimens used are serum or plasma. Urine specimen is diluted to 1:20 ratio. Do not
use hemolysed samples. Do not use ammonia – heparinate and fluorides as anticoagulants.
Urea in the serum is stable upto 3 days if stored at 2-8o c or for three months at – 20oC.
Procedure
The procedure is done at wavelength 340 nm and the working temperature was 37oC.
The reagents were brought at 15oC – 25oC before using them.
Monoreagent procedure “Sample Starter”
Blank Standard Sample
Working reagent 1000  l 1000  l 1000  l
Distilled water 10  l - -
Sample - - 10  l
Standard - 10  l -
All the reagents were prepared as above and incubated at 37oC. After 30 minutes of
addition of the sample the absorbance values of first reading was taken as E1C and standard
was taken as E1 Std. After 60 minutes the absorbance value of second reading was taken as
E2 C and that of standard was taken as E2 STD.
Calculation
S. Urea is calculated as,
E2C  E1 C 
S.Urea (mg/dl) = xConc. Std
E2 Std  E1 std 
For diluted urine – Multiply the result with dilution factor.
Conversion factor
Urea (mg/dl) x 0.1665 = Urea (mmol/l)
Reference values
Serum Urea = 10 – 50 mg/dl (OR) 1.67 – 8.32 mmol/l
Urea in Urine = 20-35g/24 hour (OR) 3330583 mmol/24hour
Linearity
The reaction is linear upto a concentration of 300 mg/dl (49.95 mmol/l) with a range
of 4.9-300 mg/dl (0.81 – 49.95 mmol/l). Samples with values exceeding 300 mg/dl must be
diluted with saline solution. Then multiply the result for dilution factor.
ESTIMATION OF SERUM CREATININE
The method used for estimation of creatinine in serum or urine was Jaffe’s
calorimetric method without deproteinization.

Principle
Creatinine reacts with picrate in alkaline environment to give a coloured compound
whose intensity is proportional to the creatinine concentration in the sample.
Components
Reagents Concentration
R1 : Lithium hydroxide 120 mmol/l
Boric acid 80 mmol/l
R2 : Picric acid 67 mmol /l
Reagents are liquid and ready to use. For using as monoreagent (sample starter
procedure) the reagents R1 and R2 were mixed in equal parts. After opening the vials R1 and
R2 are stable for 90 days if recapped immediately and protected form contamination,
evaporation, direct light and stored at correct temperature.
Specimen collection
Serum or plasma and urine. Do not use hemolysed samples. The creatinine is stable
in the samples up to 24 hours at 2-8oC.
Procedure: (Mono reagent ) Procedure “Sample starter”
Wavelength 510 nm
Working temperature 37oC
Reaction – fixed time

Working reagent 1000  l 1000  l 1000  l
Distilled water 50  l - -
Sample - - 50  l
Standard - 50  l -
The reagents were mixed as above and incubated at 37oC. After 30 minutes the
absorbance of sample (E1C) and standard (E1 std) was read against the reagent blank. After
another one minute the second reading was taken as E2C and E2 std.
Calculation
E2C  E1 C 
S. Creatinine (mg/dl) = xConc. Std
E2 Std  E1 std 
Conversion factor
S.Creatinine (mg/dl) x88.4 = S.Creatinine (  mol/l)
Reference intervals
S.Creatinine in males is 0.9 – 1.3 mg/dl (80-115  mol/l)
In females 0.6-1.1 mg/dl (53-97  mol/l)
ESTIMATION OF URINE CREATININE
The same procedure was followed but the sample urine (100  l) was diluted with
900  l distilled water. The same procedure was done using 500  l of creatinine reagent
and 50  l of diluted urine.
Reference interval
Normal urine creatinine is 60-130 mg/dl.
ESTIMATION OF SERUM CALCIUM
Serum calcium was estimated using calcium Bio systems kit.
Principle
Calcium in the sample reacts with arsenazo III forming a coloured complex which can
be measured by spectrophotometry.
Contents
A.Reagent - Arsenazo III 0.2 mmol /l
- Imidazole 75 mmol/l
S.Standard - Calcium / magnesium standard
Calcium 10mg/dl, Magnesium 2mg/dl
Aqueous primary standard.
Sample: Serum
Calcium in Serum / plasma is stable for 10 days at 2-8oC. Anticoagulants other than
heparin should not be used.

Procedure
Calcium Standard (S) - 15 µL -
Sample - - 15 µL
Reagent (A) 1000 µL 1000 µL 1000 µL
The reagent was brought to room temperature 500  l of the reagent was taken and
10  l serum was added to it and mixed well and then incubated at room temperature for 5
mts and the value was taken in a semiautoanalyzer.
Reference Range
Serum calcium is 8.6 – 10.3 mg/dl = 2.15 – 2.58 mmol/lt
ESTIMATION OF SERUM PHOSPHORUS
Method used was molybdate /UV method
Principle: End point Analysis. Inorganic phosphorous reacts with Ammonium molybdate in
acid environment to form phospho molybdate complex. The increase in absorbance is
proportional to the inorganic phosphorous in the sample.
Constituents of the reagent
Reagent Concentration
Hydrochloric acid 1.0 mmol/L
Ammonium Molybdate 0.70 mmol/L
Surface active agents Anionic and poly anionic

Specimen: Serum/ Plasma
Procedure
Reaction type - End point
Wave length - 340 nm
Temperature - 37oC
Incubation - 5 minutes at room temperature
Working reagent was prepared 250  L of reagent 1 and 250  l of reagent 2 were
mixed well. (This reagent is stable for 2 days at 2-8oC).
BLANK STD SAMPLE
Working reagent 1000  L 1000  L 1000  L
Distilled Water 10  L - -
Sample - - 10  L
Standard - 10  L -
Mix, then incubate for one minute at 37o C. Measure the absorbance of the sample (EC)
and standard (ESTD) against the reagent blank.
Reference interval
Children 4 - 7 mg/dl
Adults 2.5 – 5 mg/dl

COLOUR PLATES
C.P 1Collection of Venous blood sample
C.P 2 Various blood collection tubes

C.P 3 Table top centrifuge
C.P 4 Separation of serum

C.P 5 Semi auto analyzer
C.P 6 Structure of alpha amylase

C.P 7 Action of alpha amylase
C.P 8 Mechanism of action of lipase

RESULTS AND OBSERVATIONS
Results and observations
RESULTS AND STATISTICAL ANALYSIS

The results of the various biochemical parameters obtained on analysing the blood and urine
samples of 50 cases of chronic renal failure selected for the study were tabulated in three
different tables.
Data was entered in excel spread sheet and was analysed using statistical software Epi
Info Version3.5.3.Analysis was done by simple proportion,mean±SD and Chisquare test.
The mean and standard deviation were calculated for each of the biochemical
parameters pertaining to renal and pancreatic functions namely serum urea, serum creatinine,
urine creatinine, creatinine clearance, serum amylase, urinary amylase and serum lipase in all
the three tables giving the results of mild, moderate and severe renal failure individuals. In
addition to the above parameters which would give detailed analysis of renal and pancreatic
functions, the other biochemical parameters which are involved in renal diseases like Serum
Calcium and phosphorous were also assessed to complete the study and tabulated in the
above tables.
For mild chronic renal failure individuals the mean serum urea was 58.69±9.65mg/dl
and the mean of serum and urea Creatinine was 2.52±0.26 mg/dl and 64.16±11.81mg/dl
respectively. The mean serum amylase was 158.36±31.45U/dl whereas the urinary amylase
was 101.15±25.45U/dl. The mean Creatinine clearance and amylase clearance calculated
from the above values were 57.24±14.40ml/min and 1.44±0.41ml/min respectively. The
mean ratio of amylase clearance to that of Creatinine clearance was 2.62±0.86±%.The mean
serum lipase was153.32±73.81U/L. The other parameters like serum calcium and serum
phosphorus for this group were 8.4±0.65mg/dl and 4.88±0.71mg/dl respectively.
For moderate chronic renal failure the mean serum urea was 87.09±6.02 mg/dl. The
serum Creatinine and urine Creatinine were 3.68±0.75 mg/dl and 74.59±17 mg/dl
respectively. The mean serum amylase and urinary amylase were 185.72±71.28 U/dl and
83.94±27.85U/dl respectively. The mean Ccr and Cam were 26.44±5.6 ml/min and
0.62±0.25ml/min respectively. Cam/Ccr ratio was found to be 2.39±0.92%. The mean serum
lipase was 166.53±99.64U/L. The mean serum calcium and phosphorous were
8.19±0.46mg/dl and 5.07±0.62mg/dl respectively.
The results of severe chronic renal failure patients are as follows. The mean serum
urea, serum and urinary Creatinine were 142.02±38.56mg/dl, 7.39±2.56mg/dl and
61.27±15.22mg/dl respectively. The mean values of serum and urinary amylase were
196.21±44.39U/dl and 86.10±17.51U/dl respectively. The Ccr and Cam calculated from the
above values were 7.11±4.01ml/min and 0.34±0.13ml/min respectively. The Cam/Ccr ratio
was found to be 5.67±2.22%. The mean value of serum lipase was 168.17±71.68U/L. The
mean serum calcium and phosphorous were 8.18±0.29mg/dl and 5.41±0.5.1mg/dl
respectively.
To understand the significance of assessing the serum and urinary pancreatic enzymes
and the ratio of amylase to Creatinine clearance in renal failure, these parameters as well as
the other parameters assessed for renal failure(serum calcium and phosphorous) are
compared between various grades of renal failure in the following tables.

Table 1 Comparison between mild and moderate renal failure
Serum Urinary Amyla 𝑪𝒂𝒎 Serum Serum Serum

%
Amylase amylase se 𝑪𝒄𝒓 Lipase Calciu phosphor
U/100ml U/100ml clearan U/L m ous
ce mg% mg%
(Cam)
ml/min
Mild
158.36±31 101.15±25 1.44±0. 2.62±0. 153.32±73 8.4±0.6
renal 4.88±0.71
.45 .45 41 86 .81 5
failure
Moderat
185.72±71 83.94±27. 0.62±0. 2.39±0. 166.53±99 8.19±0.
e renal 5.07±0.62
.28 85 25 92 .64 46
failure
T-value 2.08 3.44 47.05 0.56 0.19 1.17 0.68
P-value 0.16 0.07 0.00 0.46 0.67 0.29 0.42
Significa
NS NS S NS NS NS NS
nce
Table 1 shows the comparison of parameters between mild and moderate renal failure
Here we found out that the T value for serum amylase was 2.08, for urinary amylase
was 3.44, for serum lipase was 0.67, for serum calcium was 0.29, for serum phosphorous was
𝑪𝒂𝒎
0.68 and for % was 0.56. Their P values were >0.05 and hence were not of significance.
𝑪𝒄𝒓
But for amylase clearance T value was 47.05 and the P value was 0.000(<0.01) which
showed a significant variation.

Table 2Comparison between moderate and severe renal failure
Serum Urinary Amylas 𝑪𝒂𝒎 Serum Serum Serum

%
Amylase amylase e 𝑪𝒄𝒓 Lipase Calciu phosphor
ce mg% mg%
(Cam)
ml/min
Moderat
185.72±71 83.94±27. 0.62±0. 2.39±0. 166.53±99 8.19±0.
e renal 5.07±0.62
.28 86 25 92 .64 46
failure
Severe
196.21±44 86.1±17.5 0.34±0. 5.67±2. 168.17±71 8.18±0.
renal 5.40±0.51
.39 1 13 22 .68 29
failure
T-value 0.26 0.07 17.19 30.58 0.003 0.002 2.93
P-value 0.61 0.79 0.00 0.00 0.96 0.97 0.1
Significa NS NS S S NS NS NS
nce
Table 2 shows the comparison of biochemical parameters between moderate and severe renal
failure. Here the T values for all the parameters compared were serum amylase – 0.26,
urinary amylase – 0.07, serum lipase – 0.003, serum calcium – 0.002 and serum phosphorous
– 2.93. Their P values were >0.05 and hence were not significant. But the T values for
𝑪𝒂𝒎
amylase clearance was 17.192 and for % was 30.58 whose P values were 0.00(> 0.01)
𝑪𝒄𝒓
which showed a significant variation.

Table 3 Comparison between mild and severe renal failure
Serum Urinary Amyla 𝑪𝒂𝒎 Serum Serum Serum

%
Amylase amylase se 𝑪𝒄𝒓 Lipase Calciu phosphor
ce mg% mg%
(Cam)
ml/min
Mild
158.36±31 101.15±25 1.44±0. 2.62±0. 153.32±73 8.4±0.6
renal 4.88±0.71
.45 .45 41 86 .8 5
failure
Severe 8.18±0. 5.41±0.51
196.21±44 86.1±17.5 0.34±0. 5.67±2. 168.16±71
renal 29
.39 0 13 22 .68
failure
T-value 8.23 4.04 112.19 27.86 0.35 1.60 6.21
P-value 0.01 0.05 0.000 0.000 0.56 0.22 0.02
Significa S NS S S NS NS S
nce
Table 3 shows the comparison of all the parameters between mild and severe renal failure.
Here we found out that T values for urinary amylase was 4.04., for serum lipase it was 0.35
and for serum calcium it was 1.6. Their P values were>0.5 and showed no significance.
But the T value for serum amylase was 8.23 and the P value was 0.007(<0.05) which
showed significant variation. Similarly the T value for amylase clearance was 112.19 and
𝑪𝒂𝒎
% was 27. 86 and their P values were 0.000(<0.01) which showed significant variation.
𝑪𝒄𝒓
The T value for serum phosphorous was 6.21 and its P value was 0.02(<0.05) which also
showed significant variation.

Table 4 Correlation of serum amylase and serum urea in various study groups
Mild renal Moderate Severe renal

failure renal failure failure
Serum Urea(mg%) 58.69±9.65 87.09±6.02 142.02±38.56
Serum
158.36±31.45 185.72±71.28 196.21±44.39
Amylase(U/100ml)
Pearson correlation
0.33 -0.11 -0.03
Coefficient
p-Value 0.20 0.69 0.92
Significance NS NS NS
To find out the correlation level of each of the pancreatic enzymes with that of serum
urea or serum Creatinine which are the two most important parameters of renal function,
Pearson correlation coefficient was obtained by comparing their level in various study groups
like mild, moderate & severe renal failure & the significance of the same was obtained.
In Table 4 Correlation between serum urea and serum amylase has been made in
various study groups mild, moderate and severe renal failure respectively. The P value
derived from the Pearson correlation coefficient on comparison of the parameters in various
study groups showed that serum amylase had no significant correlation P (>0.05), with
serum urea in all the study groups.

Table 5 Correlation of serum lipase and serum urea in various study groups
Mild renal Moderate renal Severe renal

failure failure failure
SERUM
58.69±9.65 87.09±6.02 142.02±38.56
UREA(mg%)
Serum
153.32±73.81 166.53±99.64 168.17±71.68
Lipase(U/L)
Pearson
correlation 0.12 -0.27 0.09
Coefficient
P-Value 0.66 0.31 0.72
In Table 5 a comparison has been made between serum lipase and serum urea in various
study groups mild, moderate & severe renal failure respectively. The P value derived from
the Pearson correlation coefficient on comparison of the parameters in various study groups
showed that serum lipase had no significant correlation ( P>0.05) with serum urea in various
study groups.
Table 6 Correlation of serum creatinine and serum amylase in various study groups

Serum
Creatinine 2.52±0.26 3.68±0.63 7.39±2.56
(mg%)
Serum
Amylase(U/100 158.36±31.45 185.72±71.28 196.21±44.39
ml)
Pearson
correlation 0.37 0.65 0.25
Coefficient
P-Value 0.14 0.01 0.34
Significance NS HS NS
Table gives a comparison of serum amylase with serum Creatinine in various study groups
mild, moderate & severe renal failure. The P value was derived from Pearson correlation
coefficient by comparing the parameters in various study groups, The P vale was >0.05 when
serum amylase was compared serum Creatinine in mild & severe renal failure, but the P value
was 0.01 in moderate renal failure which showed significance.

Table 7 Correlation of serum creatinine and serum lipase in various study groups
MILD RENAL MODERATE SEVERE

FAILURE RENAL RENAL
FAILURE FAILURE
Serum Creatinine
2.52±0.26 3.68±0.631 7.39±2.56
(mg%)
Serum Lipase (U/L) 153.37±73.81 166.53±99.64 168.17±71.68
Pearson correlation
0.05 0.45 0.21
Coefficient
P-Value 0.84 0.08 0.43
Table 7 gives a comparison of serum lipase with serum Creatinine in various study groups
mild, moderate & severe. The P value was derived from Pearson Correlation coefficient by
comparing these parameters in all the study groups. The p value was not significant (>0.05)
when serum lipase was compared with serum Creatinine in all the study groups.
Table 8 Correlation of serum creatinine and amylase clearance in various study groups
MILD RENAL MODERATE SEVERE

FAILURE RENAL RENAL
FAILURE FAILURE
Serum Creatinine
2.52±0.26 3.68±0.63 7.39±2.56
(mg%)
Amylase clearance
1.44±0.41 0.62±0.25 0.34±0.13
(ml/min)
Pearson correlation
-0.06 -0.54 -0.64
Coefficient
P-Value 0.82 0.03 0.01
Significance NS S HS
Table 8 shows the correlation of serum Creatinine & amylase clearance in various
study groups – mild, moderate & severe renal failure respectively. The P value was derived
from Pearson correlation coefficient by comparing the parameters in various study groups.
The P value was >0.05 when serum Creatinine was compared to amylase clearance in mild
RF, but the P value was <0.05 in moderate RF & <0.01 in severe RF which showed two
tailed significance.
𝑪𝒂𝒎
Table 9 Correlation of serum creatinine and ratio in various study groups
𝑪𝒄𝒓

Serum Creatinine
2.52±0.26 3.68±0.63 7.39±2.56
(mg%)
𝑪𝒂𝒎
% 2.62±0.86 2.39±0.92 5.6741±2.22
𝑪𝒄𝒓
Pearson correlation
0.45 -0.41 0.56
Coefficient
P-Value 0.07 0.12 0.02
Significance NS NS S
Table 9 Shows a correlation between serum Creatinine & Cam ration in various study
groups –mild, Moderate & severe renal failures respectively. The P value was derived from
Pearson correlation coefficient by comparing these parameters in all the study groups. The P
value was found to be >0.05 in mild & moderate renal failure which showed no significance.
The P value was <0.05 in severe renal failure which showed significance.
Table 10 Correlation of serum creatinine and serum calcium in various study groups

Serum Creatinine
2.52±0.26 3.68±0.63 7.39±2.56
(mg %)
Serum calcium
8.4±0.65 8.19±0.46 8.18±0.29
(mg %)
Pearson correlation
0.04 -0.42 0.12
Coefficient
P-Value 0.87 0.11 0.65
Table 10 shows the correlation between serum Creatinine & serum phosphorous in various
study groups mild, moderate & severe renal failure. The P value was derived from Pearson
correlation coefficient by comparing the parameters in various study groups. The P value was
>0.05 when serum Creatinine was compared with serum phosphorous in mild& severe renal
failure which showed no significance, but in moderate renal failure the P value was <0.01
which showed two tailed significance.

Table 11 Correlation of serum creatinine and serum phosphorus in various study groups

Serum Creatinine
2.52±0.26 3.68±0.63 7.39±2.56
(mg %)
Serum Phosphorus
4.88±0.71 5.07±0.62 5.41±0.51
(mg %)
Pearson correlation
0.14 0.74 0.05
Coefficient
P-Value 0.59 0.00 0.86
Significance NS HS NS
Table 11 shows the correlation between serum Creatinine & serum calcium in various study
groups- mild, moderate & renal failure respectively. The P value was derived from the
Pearson correlation coefficient. The P value was found to be >0.05 in all the study groups
which showed no significance.

Table 12 Correlation of serum calcium and serum phosphorus in various study groups

Serum Calcium (mg
8.4±0.65 8.19±0.46 8.18±0.29
%)
Serum Phosphorus
4.88±0.71 5.07±0.62 5.41±0.51
(mg %)
Pearson correlation
-0.57 -0.45 -0.23
Coefficient
P-Value 0.02 0.07 0.37
Significance S NS NS
Table 12 shows the correlation of serum calcium & serum phosphorous in various study
groups – mild, moderate & severe renal failure respectively. The P value was derived from
the Pearson correlation coefficient. The P value was <0.05 in mild renal failure which showed
significance, but the P value was >0.05 in moderate & severe renal failure which showed no
significance.
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A Study About The Changes in Levels of Pancreatic Enzymes in Cases of Chronic Renal Failure

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A STUDY ABOUT THE CHANGES IN LEVELS OF

PANCREATIC ENZYMES IN CASES OF CHRONIC

Submitted to The Tamilnadu Dr.M.G.R Medical

University in partial fulfilment of the requirements for the

LEVELS OF PANCREATIC ENZYMES IN CASES OF CHRONIC RENAL

Dr.M.G.R. MEDICAL UNIVERSITY, CHENNAI, in partial fulfillment for the degree of

award of any other degree or diploma.

Dr. S. Jaya, (Guide) Dr. J. K. Sathya Sudha Devi, (Co-Guide)

I am extremely thankful to my guide Dr.S.Jaya, Professor, Department of Biochemistry

I am very grateful to Dr.Velayuthan Nair, M.B.B.S, M.S. Chairman and

I am extremely thankful to Dr.Pethuru,MD, Assistant Professor, Department of

Sl. No. Index Page No

4 List of colour plates

8 Aims and Objectives

10 Materials and methods

11 Results and observations

13 Summary and conclusion

CRF Chronic Renal Failure

GFR Glomerular Filtration Rate

ml/mt Milli litre / minute

ml/mt/m2 Milli litre per minute per metre square

CKD Chronic Kidney Disease

AFR Acute Renal failure

ESRD End Stage Renal Disease

AER Albumin excretion

EGFR Estimated Glomerular Filtration Rate

USA United States of America

SLE Systemic Lupus Erythematosis

BUN Blood Urea Nitrogen

CO2 Carbon di Oxide

G-6-P DH Glucose-6-Phosphate Dehydrogenase

RBC Red Blood Corpuscles

FSH Follicle Stimulating Hormone

ECF Extra Cellular Fluid

mmol/lit Milli mole / liter

mmol Milli mole

PTH Parathyroid Hormone

S.amylase Serum Amylase

K.Da Kilo Dalton

RES Reticulo Endothelial System

U/L Units per liter

Mg/dl Milligram per deciliter

ng/day Nanogram per day

Cam Amylase clearance

Ccr Creatinine clearance

Mg% Milligram percentage

mmol/L Millimole per litre

IU/L International units per litre

CNP Chloro nitro phenol

ERCP Endoscopic Retrograde Cholangio Pancreatography

Table No. Title

Table 1 Comparison between mild and moderate renal failure

Table 2 Comparison between moderate and severe renal failure

Table 3 Comparison between mild and severe renal failure

Correlation of amylase clearance and serum creatinine in various study

Correlation of serum phosphorous and serum creatinine in various study

Graph No. Title

Graph 1 Comparison of serum amylase in various study groups

Graph 2 Comparison of urinary amylase in various study groups

Graph 3 Comparison of Cam in various study groups

Graph 5 Comparison of serum lipase in various study groups

Graph 6 Comparison of serum calcium in various study groups

Graph 7 Comparison of serum phosphorous in various study groups