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Diabetic Nephropathy Chronic Glomerulonephritis Chronic Pyelonephritis

Pathophysiology of Chronic Renal Polycystic Kidney Dse. HPN Nephrosclerosis Systemic Lupus Erythematosus

Intracellular Glucose
Failure 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
glomerulus Ischaemia, Nephron loss, Renal Blood their corresponding antigen
Shrinkage of Kidney
Renal blood vessels &
Stage Renal Reserve nephrons are compressed &
obstructed & functional tse. Forms Immune Complexes
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 BUN, 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%
Sharp
Stage Renal Failure BUN,

Impaired kidney function & Uremia

Na & H2O K+
HCO3 H +
Nitrogenous Erythropoietin Mg +
Vit. D Phosphate Toxins Toxins impair Salivary Deposit of Toxins affect the Toxins causes Retentio
retention retention production retention waste production retention activation retention Continuous decline in renal fxn. irritate WBCs, humoral & urea urea on nerve fibers CNS affectation n of
in kidney impairs pericardial cell mediated breakdown skin
platelets sac immunity;
Hyperkalemia Hyper- Hyperphosphatemi > 90% kidney Fever is Atrophy & Uremic Cells become
Urine  magnesemia suppressed; Uremic  Uremic Demyalination Encephalopathy resistant to
Output Blood Metabolic GI Bleeding Pericarditi Fetor Frost insulin
Phagocyte becomes
Acidosis stress tendencies Anemia Ca+  Reduction in renal capillaries
defective Peripheral Reduction in
absorption  Scarring of Glomeruli 
Oliguria  Atrophy & Fibrosis of Cardiac Irritation of Neuropathy alertness & Erratic blood
Malfunction Lungs tubules Tamponade Phrenic awareness glucose level
of RAAS Compensates GI Blood loss Hypo- Immune  Changes in
bleeding during calcemia System Decline Restless Leg mentation
hemodialysis Stage End Stage Renal Dse. Hiccups Syndrome Because of
 Difficulty of
Kussmaul’s (ESRD) glucose
Parathyroid GFR less Risk for Superinfection concentrating
Respiration intracellularly,
overworks than 10%  Fatigue
liver produces
Edema Heart  Loss of (Hyperpara- Continuous Multisystem  Insomnia
 tryglycerides
Failure  Anorexia appetite thyroidism) Affectation  Psychiatric
& HDL
 Nausea symptoms
 Vomiting
 Gastroenteri  Fatigue PTH secretion Death
tis  Weakne
ss Atherosclerosis
 Peptic Ulcer
Pulmonary Edema Ca+ resorption
Peripheral Edema from bone +
Ca absorption
from GI tract Thrombus
& Embolus
Formation
Renal Osteodysthrophy

 Osteomalacia By: Jonnel Montoya Musngi


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