CKD

Define CKD

≥3 months of kidney damage (albuminuria, structural abnormalities) or decreased kidney function (eGFR <60).

Normal GFR=___. Kidney Failure GFR=___.

Normal= 125ml/min. Kidney failure=<15ml/min

Most common causes of CKD in US

Diabetes (≈45%), HTN/vascular (≈28%), glomerular diseases, cystic disease.

Define albuminuria categories

Normal <30 mg/day. Micro= 30-300mg/day. Macro= >300mg/day

Mechanism of CKD progression

Nephron loss → hyperfiltration → glomerular HTN → proteinuria → inflammation → fibrosis → GFR decline.

How proteinuria worsens CKD

Tubular protein overload → cytokines, macrophages, ROS → interstitial fibrosis → nephron loss.

Role of ACEI/ARB in CKD

↓ intraglomerular pressure + ↓ proteinuria → slows CKD progression.

Best predictor of GFR decline? Tx?

Proteinuria(>3.5g/day). Tx with ACE/ARBs

Risk factors for CKD progression

Proteinuria, HTN, DM, PKD, African ancestry(APOL1 gene), male sex, obesity, smoking, high phosphate, acidosis.

Why CVD is common in CKD? What is Leading Cause of death in CVD?

HTN, dyslipidemia, inflammation, vascular calcification, anemia → leading cause of death.

Cause of anemia in CKD

↓ EPO production (due to damaged nephrons>production comes from PT), iron deficiency, inflammation, shortened RBC survival(esp dialysis pts), platelet dysfunction(uremic).

Treatment of anemia in CKD

Correct iron deficiency → consider Erythrocyte Stimulating Agent(ESA) if Hgb <10

Pathophysiology of secondary hyperparathyroidism

Decreased GFR→Phosphate retention → ↑FGF23(to remove phosphate) → ↓1,25D(FGF suppresses it) → hypocalcemia → ↑PTH(to maintain nromal calcium level). »Eventually low Ca and high Phosphate

Complications of secondary hyperparathyroidism

Renal osteodystrophy(Ca pulled from bones), fractures(Ca pulled from bones), vascular/soft tissue calcification(Ca deposits in vessels), pruritus, myopathy.

Treatment of secondary hyperparathyroidism

Control phosphate (diet + binders), correct Vit D deficiency, active Vit D analogs, calcimimetics(mimics Ca to dec PTH), parathyroidectomy if refractory.

Cause of metabolic acidosis in CKD

↓ acid excretion → H+ retention → serum bicarbonate 12–20.

Consequences of metabolic acidosis in CKD

Bone resorption, muscle catabolism, worsened CKD progression.

Treatment of metabolic acidosis in CKD

Oral bicarbonate to maintain HCO₃⁻ >22.

Define uremia

Clinical syndrome from retained toxins in advanced CKD (fatigue, nausea, pruritus, neuropathy, pericarditis, sallow skin, peripheral neuropathy).

Symptoms of uremia

Fatigue, anorexia, dysgeusia, pruritus, nausea, neuropathy, restless legs, cognitive changes.

Signs of uremia

Asterixis, pericarditis, platelet dysfunction, sallow skin, malnutrition.

Treatment of uremia

Dialysis or transplant — only definitive therapy.

Mainstays of CKD management

Control BP, reduce proteinuria, treat anemia, manage phosphate/PTH, correct acidosis, statins, glycemic control, lifestyle.

Primary Vs Secondary Hyperparathyroidism

Primary= due to overactive Parathyroid, normal to low Phosphate, High calcium
Secondary= due to renal compensation mechanism, High Phosphate (due to low GFR), low calcium