CONSEQUENCE
MECHANISM
FINDINGS
MANAGEMENT · CLUE
Diabetic nephropathy, hypertensive nephrosclerosis, glomerulonephritis, ADPKD, obstruction
Staged by GFR and albuminuria; small, scarred kidneys (except DM, ADPKD, amyloid, HIV)
ACEi/ARB, SGLT2i slow progression
↓ erythropoietin from peritubular interstitial cells
Normocytic normochromic anemia, low reticulocytes
Iron + ESA (epoetin) · ESA → hypertension, thrombosis
↓ phosphate excretion + ↓ 1α-hydroxylase (↓ calcitriol) → ↓ Ca²⁺, ↑ PO₄³⁻, ↑ FGF23 → secondary hyperparathyroidism
Renal osteodystrophy: osteitis fibrosa cystica, osteomalacia, adynamic bone; vascular calcification
Phosphate binders (sevelamer), calcitriol, cinacalcet
Tertiary hyperparathyroidism
Long-standing stimulation → autonomous parathyroid hyperplasia
↑↑ PTH with high calcium
Parathyroidectomy
↓ ammoniagenesis and H⁺ excretion; later retained anions
Normal anion gap early → high anion gap late
Oral bicarbonate · acidosis worsens bone loss
↓ K⁺ excretion; worsened by ACEi, ARB, spironolactone, NSAIDs
Peaked T waves, weakness, arrhythmia
Calcium gluconate, insulin + glucose, binders, dialysis
Na⁺ and water retention, ↑ renin
Hypertension, edema, heart failure, LVH
Loop diuretics, salt restriction
Retained nitrogenous toxins
Nausea, anorexia, pruritus, pericarditis, encephalopathy, asterixis, neuropathy, uremic frost
Indication for dialysis
Uremic toxins impair platelet function (vWF–GpIb interaction)
↑ bleeding time with normal platelet count, PT and PTT
Desmopressin, dialysis
Accelerated atherosclerosis, vascular calcification, LVH
MI, stroke, sudden death — leading cause of death in CKD
Statins, BP control
↓ renal clearance
Adjust: aminoglycosides, vancomycin, digoxin, lithium, LMWH, gabapentin
Metformin → lactic acidosis at low GFR
β₂-microglobulin not cleared; long-term dialysis
Dialysis amyloid (carpal tunnel, arthropathy), acquired cysts (→ RCC), calciphylaxis (painful necrotic skin)
Transplant → see rejection (
2.09)