Renal Physiology

Renal Physiology
Nephron: Renal Corpuscle
(Glomerulus) + Renal tubule
Cortical nephrons: cannot concentrate urine
as much, don't go deep into medulla
Jextamedullay nephrons: make concentrated
urine-go deep into medulla
Nephron structure
Disease
ACUTE RENAL FAILURE: Abrupt decline in GFR & accumulation of nitrogenous waste (creatinine + urea). COMPLICATIONS: Fluid overloas, pulmonary oedema, heart failure, hyperkalaemia.
Pre-Renal: SHOCK, Hypovolaemia, Renal artery stenosis.
Test: bland urinary sedement (little protein/cells, high serum urea compared to creatinine.
Intra-renal:
Tubulo-interstitial: 1) Acute tubular necrosis (usually resolves), from unresolved pre-renal problem 2) Interstitial nephritis: DRUGS like penicillins, aspirin, NSAIDS (Analgesic nephropathy).
Glomerular (presence of haemeturia, lipiduria & proteinuria): glomerularnephritis is usual cause & is divided into types:
1) Nephritic Syndrome: inflammatory condition associated with low urine volume & haematuria
2) Nephrotic Syndrome: associated with high proteinuria & caused from diseases such as Diabetes, Hep B, HIV, Obesity. Also associated with hyperlipidemia & oedema.
Vascular: Hypertension, Polyarteritis
Post-renal: Bladder outflow obstruction, neurogenic bladder, urethral stricture, ureteric obstruction (stone), carcinoma
Test: Hydronephrosis on abdominal U.S
CHRONIC RENAL FAILURE: Stage 1: GFR>90 Stage 4: GFR=15-29 Stage 5: GFR=<15% End Stage: GFR=<10% GFR
Causes: Diabetic Nephropathy (most common), Glomerulonephritis (unresolved acute form), Vascular dx, Obstructive uropathy
Consequences: CVS (WORSE): Hypertension goes with CFR, accelerated atherosclerosis, cardiac failure. Proteinurea is a VERY STRONG RISK FACTOR for CVS Death GIT (anorexia, nausea, vom), Resp (Acidosis, pulmonary oedema), Neuro (confusion, coma, peripheral), Derma (Pruritis, leukonichia), Musculo (muscle wasting, renal bone dx (hypocalcaemia)
DRUGS
No. 1: ACE INHIBITORS to disrupt renin-angiotensin system. ACts as an antihypertensive, anti A.M.I
Biochemical tests of renal function
Urinanalysis: for glucose, creatinine, drugs,
GFR Measurement: via creatinine, as they are freely filtered & not absorbed. Can compare blood creatinine vs urine creatinine. If ratio is high then decreased GFR & renal function. Good for comparing before & after of one patient, but not good for between pt's.
Renal Plasma Flow: Use measurement of substance PAH as it is secreted by the tubules & only 20-30% filtered by glomerulus. 10% of plasma flow though goes to non-functioning parts of kidney.
Bicarbonate Handling
Drugs: Diuretics
Reabsorption along different parts of the Nephron
Urine Formation
Composition: 95% water + urea Nitrogenous waste=uric acid +creatinine
Na+ Reabsorption
2 Steps:
2) Na+/K+/ATPase pumps move Na+ into capillary & K+ into tubular cell then into lumen by diffusion
Glucose Reabsorption
2 Steps:
1) Co-symporter with Na+
2) Via Secondary Active Transport. Energy from Na+/K+/ATP pump facilitates glucose moving against its concentration gradient into capillary
Transport Maximum
Transport Maximum (Tm): when there is saturation of available carrier molecules for a particular solute.
Green graph shows normal glucose reabsorption. Orange graph shows Transport maximum being met, at which point, purple graph shows proportion of glucose that is then excreted into the urine. As amount of glucose entering kidneys increases, more & more is excreted until at the point of graph intersection, more glucose is being excreted than absorbed. This is the case in diabetic patients where high levels of blood glucose mean carrier molecules are quickly saturated.
1) PASSIVE carrier mediated facilitated diffusion (channel) into tubular cell
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