Anatomy and Pathophysiology of the Kidney: Nephron, Filtration, and Diabetes

What is the path of urine through the kidney?

Cortex → Medulla (pyramids) → Calyces → Pelvis → Ureter.

What is the order of the nephron?

Bowman's capsule → proximal tubule (PCT) → loop of Henle → distal tubule (DCT) → collecting duct.

What are the three layers of the filtration barrier?

Fenestrated endothelium → basement membrane (negatively charged, repels albumin) → podocyte slit diaphragms.

What is the difference between afferent and efferent arterioles?

Afferent arrives at the glomerulus, efferent exits it. Constricting the efferent raises glomerular pressure.

What does the PCT reabsorb?

About 65% of Na⁺ and water, plus nearly all glucose, amino acids, and bicarbonate.

Why does glucose appear in the urine?

Filtered glucose exceeds the transport maximum (renal threshold ≈ 180 mg/dL), causing osmotic diuresis.

What causes early hyperfiltration in diabetic nephropathy?

High glucose increases SGLT2 activity, reducing NaCl at the macula densa, leading to GFR rise.

What is the histology of diabetic nephropathy?

Thickened basement membrane, mesangial expansion, and Kimmelstiel-Wilson nodules.

What is the earliest clinical sign of diabetic nephropathy?

Microalbuminuria: urine albumin-to-creatinine ratio (ACR) of 30-300 mg/g.

Why are ACE inhibitors/ARBs used in diabetic kidney disease?

They block angiotensin II, dilating the efferent arteriole, lowering intraglomerular pressure.

How do SGLT2 inhibitors protect the kidney?

They block PCT glucose reabsorption, leading to glycosuria and restoring tubuloglomerular feedback.