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Topic 6

Part of the FMGE study roadmap. Botany topic physio-006 of Botany.

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Renal Physiology

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Renal Physiology — Key Facts for FMGE Core concept: The kidneys regulate fluid balance, electrolyte balance, acid-base balance, and blood pressure; they also excrete metabolic waste products High-yield point: GFR is the best measure of kidney function; clearance concepts help understand how substances are handled by kidneys ⚡ Exam tip: Know what each segment of the nephron does to water and solute handling - this is fundamental to understanding diuretics and kidney function

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Renal Physiology — FMGE Study Guide

Nephron Structure

Nephron Components

  • Glomerulus: Filter blood (capillaries between afferent and efferent arterioles)
  • Bowman’s capsule: Surrounds glomerulus; collects filtrate
  • Proximal tubule: Reabsorbs ~65% of filtered water and Na; most active reabsorption
  • Loop of Henle: Countercurrent multiplier; concentrates urine
  • Distal tubule: Fine-tuning of Na, K, H
  • Collecting duct: ADH affects water reabsorption; final urine concentration

Cortical and Juxtamedullary Nephrons

  • Cortical nephrons: 85%; short loops; primarily for regulation of solute and water
  • Juxtamedullary nephrons: 15%; long loops that dip into medulla; for concentration of urine

Glomerular Filtration

Filtration Barrier

  • Capillary endothelium: Fenestrated (pores) - prevents cells
  • Basement membrane: GBM - size and charge selective
  • Podocyte foot processes: Slit diaphragm - final barrier
  • Negatively charged: Prevents filtration of negatively charged proteins

GFR (Glomerular Filtration Rate)

  • Normal: 125 mL/min = 180 L/day
  • Filtration fraction (FF): GFR/RPF = 125/600 = ~20% of plasma is filtered

Forces (Starling Forces in Glomerulus)

  • Net Filtration Pressure (NFP) = (Pgc - Pbs) - (πgc - πbs)
  • Pgc (glomerular capillary hydrostatic pressure): ~60 mmHg (favors filtration)
  • Pbs (Bowman’s space hydrostatic pressure): ~18 mmHg (opposes filtration)
  • πgc (glomerular capillary oncotic pressure): ~29 mmHg (opposes filtration)
  • πbs (Bowman’s space oncotic pressure): ~0 mmHg (no protein normally)
  • NFP ≈ 10 mmHg (favors filtration)

Regulation of GFR

Autoregulation (myogenic and tubuloglomerular feedback):

  • Maintains GFR relatively constant despite changes in systemic BP (80-180 mmHg)
  • Myogenic response: Afferent arteriole responds to stretch by contracting
  • Tubuloglomerular feedback (TGF): Macula densa senses NaCl at distal tubule → adjusts afferent arteriole tone

Hormonal/Neural:

  • Sympathetic: ↑α1 → constricts afferent/efferent → ↓GFR (severe hypotension)
  • Angiotensin II: Preferentially constricts efferent > afferent → maintains GFR (but overall ↓RBF)
  • NSAIDs: Inhibit prostaglandins → afferent vasoconstriction → ↓GFR (especially in volume depletion)

Measuring GFR

  • Inulin clearance: Gold standard (inulin is freely filtered, not reabsorbed/secreted)
  • Creatinine clearance: Approximates GFR; slight underestimation (creatinine is slightly secreted)
  • Cockcroft-Gault equation: Estimates CrCl based on age, weight, serum creatinine
  • CKD-EPI, MDRD: More accurate equations for GFR estimation

Tubular Reabsorption and Secretion

Proximal Tubule

  • Reabsorbs: 65% of filtered Na, water, glucose, amino acids, bicarbonate
  • Na/H exchanger: ~65% of Na reabsorption via this mechanism
  • Glucose reabsorption: SGLT2 (apical) + GLUT2 (basolateral); threshold ~180 mg/dL
  • Bicarbonate reabsorption: Via carbonic anhydrase; ~90% reabsorbed in PCT
  • Fluid reabsorption: Isosmotic (no net change in osmolality)
  • Krebs-Henseleit: Loop diuretics act here

Loop of Henle

Descending limb:

  • Permeable to water (aquaporins); not to NaCl
  • Water leaves → fluid becomes hypertonic
  • Thin descending limb: Very permeable to water (up to 1200 mOsm at tip)

Ascending limb:

  • Impermeable to water; actively reabsorbs Na, K, Cl (NKCC2 transporter)
  • Thin ascending limb: NaCl reabsorption; permeable to some solutes
  • Thick ascending limb: NKCC2 transporter; Na, K, 2Cl reabsorbed
  • Generates hypertonic medullary interstitium (countercurrent multiplication)
  • Lumen becomes hypotonic as it leaves (hypotonic fluid to DCT)

Loop Diuretics (Furosemide, Bumetanide):

  • Block NKCC2 → ↓NaCl reabsorption in TAL → ↓medullary osmolarity → ↓concentrating ability → diuresis

Distal Convoluted Tubule

  • Thiazide-sensitive NaCl cotransporter (NCC): Active Na/Cl reabsorption
  • No ADH effect: Cannot concentrate urine here
  • Parathyroid hormone: ↑Ca reabsorption (via TRPV5 channels)

Thiazide diuretics: Block NCC in DCT → ↓NaCl reabsorption

Collecting Duct

Cortical collecting duct:

  • Principal cells: Na reabsorption via ENaC (epithelial Na channels); K secretion
  • Aldosterone: Stimulates ENaC → Na reabsorption, K secretion
  • Intercalated cells: H secretion (H-ATPase), K reabsorption

Medullary collecting duct:

  • ADH: Increases aquaporin-2 (AQP2) insertion → water reabsorption → concentrated urine
  • Without ADH: Collecting duct impermeable to water → dilute urine (up to 50-100 mOsm)
  • With ADH: Can concentrate urine up to 1200 mOsm (maximum)

Amiloride: Blocks ENaC (↑K retention - used with thiazides/loop diuretics) Spironolactone/Eplerenone: Blocks aldosterone receptor

Clearance Concept

Definition

Clearance = (U × V) / P

  • U = urine concentration, V = urine flow rate, P = plasma concentration
  • C = Amount removed from plasma per unit time / plasma concentration

Creatinine Clearance

  • Ccr = (Ucr × V) / Pcr
  • Approximates GFR if creatinine is not secreted/reabsorbed
  • Underestimates GFR slightly because creatinine is secreted (~10-20%)

PAH Clearance

  • CPAH = (UPAH × V) / PPAH
  • PAH is filtered and secreted → approximates renal plasma flow (RPF)
  • RPF normal: ~625 mL/min
  • ERPF (effective renal plasma flow): ~300-500 mL/min

Filtration Fraction

FF = GFR/RPF = 125/625 = 0.20 (20%)

Acid-Base Balance

H⁺ Regulation

  • Filtered bicarbonate reabsorption: ~90% in PCT
  • Ammonium (NH₄⁺) excretion: Major mechanism for acid excretion
  • Titratable acids: Phosphate buffer system

Tubular H⁺ Secretion

  • Proximal tubule: Na/H exchanger (NHE3)
  • Distal nephron: H-ATPase (intercalated cells)

Acid-Base Disturbances

Metabolic acidosis:

  • ↓pH, ↓HCO₃⁻, Normal PaCO₂ (primary)
  • Compensatory hyperventilation → ↓PaCO₂
  • Causes: Lactic acidosis, DKA, renal failure, diarrhea, loss of bicarbonate
  • Treatment: HCO₃⁻ (if severe, pH <7.1)

Metabolic alkalosis:

  • ↑pH, ↑HCO₃⁻, Normal PaCO₂ (primary)
  • Compensatory hypoventilation → ↑PaCO₂
  • Causes: Vomiting, diuretic use, primary hyperaldosteronism
  • Treatment: Address cause; give NaCl/KCl

Respiratory acidosis:

  • ↓pH, ↑PaCO₂, Normal HCO₃⁻ (acute) or ↑HCO₃⁻ (chronic)
  • Causes: Hypoventilation (COPD, obesity hypoventilation, sedation)
  • Chronic: Renal compensation (↑HCO₃⁻)

Respiratory alkalosis:

  • ↑pH, ↓PaCO₂, Normal HCO₃⁻ (acute) or ↓HCO₃⁻ (chronic)
  • Causes: Hyperventilation (anxiety, high altitude, early sepsis)
  • Chronic: ↓HCO₃⁻

Anion gap: AG = Na - (Cl + HCO₃)

  • Normal: 8-12 mEq/L
  • Elevated AG: Lactic acidosis, ketoacidosis, renal failure, toxic alcohols
  • Normal AG (hyperchloremic): Diarrhea, RTA, carbonic anhydrase inhibitors

Urine Concentration

Countercurrent System

  • Loop of Henle: Countercurrent multiplier (active NaCl pumping)
  • Vasa recta: Countercurrent exchanger (preserves medullary gradient)
  • Collecting duct: ADH increases water reabsorption

Osmolality

  • Medullary interstitium: Up to 1200 mOsm/kg (max concentration)
  • Urine: Can range from 50 mOsm/kg (dilute) to 1200 mOsm/kg (concentrated)

ADH Effects

  • ↑ADH: More AQP2 channels → more water reabsorption → concentrated urine
  • ↓ADH: Fewer AQP2 channels → water stays → dilute urine

Diabetes Insipidus

  • Central: Lack of ADH production/release (pituitary surgery, trauma)
  • Nephrogenic: Kidney doesn’t respond to ADH (hypokalemia, hypercalcemia, lithium)
  • Both cause large volumes of dilute urine, dehydration risk

Potassium Balance

K⁺ Handling

  • Filtered: Freely at glomerulus
  • Reabsorbed: 90% in PCT; 10% reaches collecting duct
  • Secreted: Principal cells of collecting duct (regulated by aldosterone)
  • Aldosterone: Stimulates K secretion in principal cells

Factors Affecting K Secretion

  • ↑Aldosterone: ↑K secretion
  • ↑Urine flow rate: ↑K secretion
  • ↓Serum [K]: ↓K secretion
  • Acidosis: ↑K secretion (H⁺ enters cells in exchange for K)
  • Aldosterone antagonist (spironolactone): ↓K secretion (hyperkalemia risk)

Hyperkalemia

  • Risk: Renal failure, hypoaldosteronism, acidosis, drugs (ACEi, ARB, K-sparing diuretics)
  • ECG changes: Peaked T waves → QRS widening → VF/asystole

Hypokalemia

  • Causes: Diuretics, vomiting, Conn’s syndrome, Cushing’s
  • ECG: Flat T waves → U waves → arrhythmias

Micturition

Bladder Function

  • Detrusor muscle: Smooth muscle; contracts during urination
  • Internal urethral sphincter: Involuntary; sympathetic (α1)
  • External urethral sphincter: Voluntary; somatic (pudendal nerve)

Micturition Reflex

  • Stretch receptors in bladder wall → signals to sacral cord
  • Parasympathetic: Contracts detrusor, relaxes internal sphincter
  • Loss of voluntary control: Neurogenic bladder (spinal cord lesions)

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