Diabetic

Chronic
ChronicGlomerulonephritis
Nephropathy
Pyelonephritis Pathophysiology of Chronic Renal Polycystic Kidney Dse. HPN Systemic Lupus Erythematosus

Failure
Intracellular Glucose Multiple Bilateral Cysts Long Standing HPN Production of large variety of
Non-modifiable Risk Factors: Modifiable Risk Factors: leads to further auto antibodies against normal
Age Diet arteriosclerosis body components such as nucleic
Repeated Inflammation Gender Sedentary Lifestyle acids, RBC, platelet, and WBC
Supports the formation of Heredity Nephrotoxins As cysts fill, enlarge
abnormal glycoprotein in the & multiply, kidneys
basement membrane of also enlarge SLE antibodies react with
Ischaemia, Nephron loss,
glomerulus ΠRenal Blood their corresponding antigen
Shrinkage of Kidney
Renal blood vessels &
ΠRenal Reserve nephrons are compressed &
Stage Forms Immune Complexes
obstructed & functional tse.
Glomerulosclerosis impairs are destroyed
the filtering fxn. of the Damage to Nephrons
glomerulus thus protein
lost in urine GFR 50% Renal Parenchyma Deposited in the
50% damage Normal BUN, atrophies & become connective tse. such as
Creatinine fibrotic & scarred blood volume & kidneys

More than 75% damage

GFR 20-50% Trigger an inflammatory

Stage Renal Insufficiency ΠBUN, response and damage
Creatinine the kidney

As nephrons are destroyed, the

remaining nephrons undergo
changes to compensate for those

Remaining nephrons must filter

more solute particles from the

Hypertrophy of remaining nephrons

Nephrons cannot tolerate the work

Further damage of nephrons

80-90% damage

GFR 10-20%
Renal Failure Sharp Œ
Stage BUN,

Impaired kidney function & Uremia

Nitrogenous
ΠNa
ΠHHCO3
+
&KH2O
+
Erythropoietin Mg +
ΠVit. D Phosphate Toxins Toxins impair Salivary Deposit of Toxins affect the Toxins causes Retentio
retention
retention
retention
waste
production
production retention activation retention Continuous decline in renal fxn. irritate WBCs, humoral & urea urea on nerve fibers CNS affectation n of
impairs
in kidney pericardial cell mediated breakdown skin
platelets sac immunity;
Hyperkalemia Hyper- Hyperphosphatemi > 90% kidney Fever is Atrophy & Uremic Cells become
Œ Urine magnesemia suppressed; Uremic  Uremic Frost Demyalination Encephalopathy resistant to
Metabolic
Bleeding
GI
Blood
Output Pericarditi Fetor  Yellowish hue insulin
Phagocyte becomes
stress
AcidosisAnemia
tendencies Œ Ca+  Reduction in renal
defective
absorption capillaries Peripheral  Reduction in
Oliguria  Scarring of Glomeruli Cardiac Irritation of Neuropath alertness & Erratic blood
Malfunction
Lungs Atrophy & Fibrosis of Tamponade Phrenic glucose level
 awareness
of GI
Compensates
RAAS Blood loss Hypo- Immune  Changes in
bleeding during calcemia System Decline Restless Leg
End Stage Renal Dse. mentation
hemodialysis Hiccups Syndrome Because of Œ
Kussmaul’s Stage (ESRD)  Difficulty of
concentrating glucose
Respiration Parathyroid GFR less Risk for Superinfection
Fatigue intracellularly,
overworks than 10% 
Heart
Edema
ΠLoss of Continuous Multisystem Insomnia liver produces
(Hyperpara- 
 Anorexia
Failure appetite Affectation Psychiatric Πtryglycerides
thyroidism) 
 Nausea symptoms & Œ HDL
 Vomiting
 Fatigue
 Gastroenteritis PTH secretion Death
 Weakness
 Peptic Ulcer
 Pallor Atherosclerosis
Pulmonary Edema Ca+ resorption
Peripheral Edema from bone +
Ca absorption
from GI tract Thrombus
& Embolus
Renal Osteodysthrophy Formation

 Osteomalacia By: Jonnel Montoya Musngi

 Osteoporosis
 Bone BSN 4-B
tenderness
 Bone pain
 Muscle
Weakness