Renal Physiology Overview

Study Notes

The urinary system maintains homeostasis by regulating blood volume and composition.
Urine is concentrated to 855-1355 mOsm/L.
The urinary system excretes solutes, especially metabolic wastes.

Urine formation involves three processes: filtration, reabsorption, and secretion.
Filtration occurs in the renal corpuscle, where blood pressure forces water and small solutes into the capsular space, creating glomerular filtrate.
Reabsorption occurs as water, ions, and needed substances are reabsorbed from the filtrate into the peritubular capillaries.
Secretion is the process where substances like wastes and excess ions move from the peritubular capillaries into the renal tubules, becoming part of the urine.

Filtration is the process where blood hydrostatic pressure pushes water and solutes across the glomerular capillaries into the capsular space.
GFR (Glomerular Filtration Rate) is the amount of filtrate produced per minute in both kidneys.
Normal GFR is 105-120 ml/min.
GFR is directly related to NFP (Net Filtration Pressure), which is the difference between GBHP (Glomerular Blood Hydrostatic Pressure), CHP (Capsular Hydrostatic Pressure), and BCOP (Blood Colloid Osmotic Pressure). Normal NFP is 10 mmHg.
Filtration fraction (FF) is the fraction of renal plasma flow (RPF) that becomes glomerular filtrate. Normal FF is 16-20%.

The filtration membrane consists of three layers: fenestrations in the glomerular endothelial cells, a basement membrane including collagen and proteoglycans, and filtration slits between pedicels of podocytes.

The kidneys have two mechanisms for regulating GFR (glomerular filtration rate): myogenic mechanism and tubuloglomerular feedback.
The myogenic mechanism is a faster response that involves the smooth muscle of the afferent arteriole. Changes in blood pressure alter the diameter of the afferent arteriole to regulate the blood flow into the glomerulus.
Tubuloglomerular feedback is a slower response, involving specialized cells called macula densa that sense changes in fluid composition to alter the GFR.

The JGA is a specialized structure where the distal convoluted tubule meets the afferent arteriole.
It is crucial in regulating GFR, blood pressure, and sodium and water balance.
Components of JGA include macula densa cells and juxtaglomerular cells.

Neural regulation, involving the sympathetic nervous system, can cause vasoconstriction of afferent arterioles to conserve blood elsewhere when blood pressure is low (MAP < 65 mmHg).
This can decrease GFR.

Angiotensin II: part of the Renin-Angiotensin-Aldosterone System (RAAS). Angiotensin II increases reabsorption of Na+, Cl-, and H2O.
ADH (Antidiuretic Hormone): increases the number of aquaporins, leading to increased reabsorption of water.
ANP (Atrial Natriuretic Peptide): acts to decrease reabsorption of Na+ & H2O. Increased stretch of the atria (as occurs with elevated blood pressure) triggers release of ANP.
PTH (Parathyroid Hormone): increases calcium reabsorption.
Calcitonin: decreases calcium reabsorption.

It is in the Early Distal Convoluted Tubule that remaining (10-15%) water is reabsorbed via osmosis and some (5%) NaCl.

The late distal convoluted tubules, along with the collecting ducts, regulate the final amounts of water and solutes in the urine.
They reabsorb or excrete depending on the needs of the body.

Obligatory water reabsorption: happens in the PCT & descending limb of the nephron loop, and is considered passive.
Facultative water reabsorption: occurs in DCT and collecting duct, and is regulated by ADH levels.
Countercurrent multiplication system: involved in generating a high osmotic gradient in the renal medulla, necessary for the kidneys to produce concentrated urine.
Countercurrent exchange: mechanism for establishing and maintaining the high osmotic gradient, using the vasa recta to conserve water and solutes in the medulla.

Diabetes insipidus is an inadequate response to or production of ADH (Antidiuretic Hormone).
Symptoms include excessive urination and extreme thirst with dehydration.
Central DI is characterized by a lack of ADH production.
Nephrogenic DI is characterized by the insensitivity of the kidney tubules to ADH.
Treatment includes synthetic ADH (desmopressin) or thiazide diuretics.