Basic Science Part 1: Afferent and Efferent

Three regions of the kidney

Cortex (outer), Medulla (inner+outer), Papilla (renal calyces → drain to pelvis)

Three hormones secreted by the kidney

Renin (→ angiotensin II → aldosterone), Erythropoietin (→ RBC production), 1-α-hydroxylase (→ activates vitamin D)

Kidney failure: consequences from lost hormones

Anemia (no EPO) + low calcium (no active vitamin D). Note: clinically CKD usually causes HIGH phosphate

Two arterioles and two capillary beds of the nephron

Afferent arteriole → glomerular capillary → efferent arteriole → peritubular capillaries

Juxtamedullary nephron special feature

Long loop of Henle → concentrates urine / conserves water

% of cardiac output to kidneys

~25% (~1.25 L/min)

Blood pressure range over which renal autoregulation works

~80–200 mmHg (mean arterial pressure)

Autoregulation: what does the afferent do when BP RISES?

Constricts (opposes the change to keep flow constant)

Autoregulation: what does the afferent do when BP FALLS?

Dilates (opens inlet to maintain flow)

Core rule: constrict EITHER arteriole → RBF?

RBF always falls (total resistance up)

Constrict AFFERENT alone → GFR?

GFR falls (less pressure reaches glomerulus)

Constrict EFFERENT alone → GFR?

GFR rises (pressure backs up into glomerulus)

Angiotensin II: which arteriole preferentially? Effect on RBF/GFR?

Efferent-dominant → RBF ↓, GFR ↑

What triggers RAAS / renin release?

LOW blood pressure or low volume (hemorrhage, dehydration, hypotension)

RAAS activation cascade

Renin → angiotensin I → (ACE) → angiotensin II → aldosterone

Sympathetic (norepi/epi) effect on RBF/GFR

Constrict both (afferent-dominant/equal) → RBF ↓, GFR ↓

Endothelin effect on RBF/GFR

Constrict both → RBF ↓, GFR ↓

ANP effect on arterioles and RBF/GFR

Dilate afferent + constrict efferent → RBF ↑, GFR ↑

Why is GFR "efferent vs afferent tug-of-war" when both constrict?

Afferent constriction lowers glomerular pressure; efferent constriction raises it. Net GFR = whichever dominates

PGE2/PGI2 (prostaglandins) effect

Vasodilate (keep afferent open) → RBF ↑, protective; GFR ~unchanged

Low-dose dopamine effect

Dilate both arterioles → RBF ↑, GFR ~unchanged

High-dose dopamine effect

α1 receptors → constrict both (afferent more) → RBF ↓, GFR ↓

CHF patient + NSAID → outcome and why

Acute renal failure: CHF kidney relies on PGE2 to keep afferent dilated; NSAID blocks prostaglandins → afferent constricts

Two mechanisms of renal autoregulation

Myogenic (stretch → smooth muscle contracts) + tubuloglomerular feedback

Tubuloglomerular feedback: what structure senses the signal?

Macula densa (in the juxtaglomerular apparatus)

Tubuloglomerular feedback: what does the macula densa sense?

NaCl delivery in the tubular fluid

Tubuloglomerular feedback: full loop for HIGH BP

↑BP → ↑GFR → ↑NaCl at macula densa → releases adenosine → constricts afferent → GFR back to baseline

What does the macula densa release to constrict the afferent?

Adenosine (a vasoconstrictor)

Tubuloglomerular feedback vs RAAS: what triggers each?

Tubuloglomerular feedback = HIGH flow (local brake); RAAS = LOW pressure (body-wide BP defense)

High-protein diet → dehydration mechanism

↑ amino acids → more Na reabsorbed with them in PCT → less Na at macula densa → misread as low flow → afferent dilates → ↑GFR → water lost in urine → dehydration

Why efferent constriction raises GFR (image)

"Kink in the hose" — blocking the outlet backs pressure up inside the glomerulus