nephrology basic science High-Yield

Glomerulus

capillary tuft + Bowman's space

fenestrated endothelium → GBM → podocyte slit diaphragm

Hematuria → glomerular barrier problem

Proteinuria → glomerular filtration barrier problem

Especially:

Albuminuria → damage to GBM/podocytes

afferent vs efferent constriction (glomerulus)

afferent constriction occurs when volume is low then leading to low GFR.

efferent constriction occur when pressure inside is high _{‘GNitis/diabetic nephropathy’} , initially cause high GFR that eventually Drops.

drugs and GFR

ACEi block constrict by aldo so low pressure inside so efferent dialation so low GFR

NSAIDs block pge so afferent constriction so low GFR

= AKI

Proximal tubule

brush border

because massive reabsorption occurs here.

Histologically:

fuzzy/luminal brush border + relatively narrow lumen.

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Distal tubule

No prominent brush border.

→ clearer, more open lumen.

PCT reabsorbs largest fraction of filter.

HIGH-YIELD:

Glucose → PCT

Amino acids → PCT

Bicarbonate → PCT

Phosphate → PCT

SGLT2 ‘Empagliflozin, dapagliflozin’

block glucose & Na⁺ reabsorption so osmotic diuresis then hypoglycaemia and risk of genital infections

DCT has _{sodium-chloride symporter} NCC = Thiazides

DCT already has low water permeability so blocking channels _{would not cause massive hypovolemia} .

Hydrochlorothiazide increase Na excretion and reduce Ca urinary so treat calcium stones and nephrogenic DI _{‘over ADH response’}

collecting duct

hormone-responsive (aldosterone and ADH)isn’t controlled by minerals

Juxta-glomerular cells respond to renin

aldosterone resistance = RTA4

hyperkalemia and M acidosis = diabetic nephropathy

second collecting duct hormone

ADH act on V2 receptors inserting aquaporin2 into them and cause water reabsorption