PATHOPHYSIOLOGY OF

CHRONIC KIDNEY DISEASE

Hyperglycemia
(DM – 15 years)

Mesangial expansion
GBM thickening
Adaptive Hyperfiltration
Kidney size is normal in
and Hypertrophy
UTZ because mesangial
expansion
compensation.
Afferent vasodilation Efferent vasoconstriction

Glomerulosclerosis
Angiotensin II -
Vasoconstriction
Increased RAAS activation Hypertension
hyperglomerular (HPN – 3 years)
permeability
Na+ and
Oliguria
water
Increased filtration imbalances
Proteinuria of protein and
Activation of
macromolecules cytokines, vasoactive
substances and pro-
PCT take up protein
inflammatory cells
and initiate LEGEND:
inflammation
Clinical
Nephrotic inflammatory manifestations
and remodeling present in patient

Tubule cells to Diabetic Nephropathy

fibroblast Tubulointers titial scarring
and fibrosis

Chronic Kidney Disease

Ischemic injury leads to

nephron loss

Decreased EPO GFR Decreased Acid-base Decreased Systemic

calcitriol imbalances 1,25 diOH infections
Na and water Vitamin D
Anemia
imbalances Decreased Metabolic
Weakness, fatigue Ca2+ acidosis Decreased
Edema reabsorption Ca2+ uptake
Periorbital and
bipedal edema

Hypertension Hyperkalemia Weakness, fatigue

Proteinuria

Hyperuricemia

Hyperphospha Parathormone Bone

Osteitis Fibrosa ,
tenemia demineralization
fractures

END-STAGE
RENAL DISEASE