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Kidney Pathology and RAAS PDF

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Document Details

SufficientPentagon

Uploaded by SufficientPentagon

Josh Landers

Tags

kidney disease pathology RAAS medicine

Summary

This document discusses kidney pathology and the renin-angiotensin-aldosterone system (RAAS). It covers various aspects of kidney function, including different types of kidney injuries and diseases, and the role of RAAS in regulating kidney function.

Full Transcript

More Kidney Stuff Josh Landers PhD, DPT, PT, CSCS 3 components of the Juxtaglomerular Apparatus 1. Juxtaglomerular cells of the afferent arteriole: Synthesize and store renin, which is secreted in response to specific stimuli (i.e. low blood flow) 2. Macula Densa of th...

More Kidney Stuff Josh Landers PhD, DPT, PT, CSCS 3 components of the Juxtaglomerular Apparatus 1. Juxtaglomerular cells of the afferent arteriole: Synthesize and store renin, which is secreted in response to specific stimuli (i.e. low blood flow) 2. Macula Densa of the DCT: Sense decreased NaCl 3. Mesangial cells: form connections via actin and microtubules which allow for selective vasoconstriction/vasodilation of the afferent and efferent arterioles with mesangial cell contraction. Macula Densa Cells Paracrine factors: adenosine and ATP üAct on nearby juxtaglomerular cells and mesangial cells to regulate renin secretion and hemodynamics of the afferent arteriole Aliskiren is the only renin inhibitor Acute Kidney Injury Prerenal vVolume depletion (hemorrhage, severe burns, diarrhea, emesis) vCardiovascular disease (heart failure, acute coronary syndrome) vMeds (NSAIDS, ARBs, ACE inhibitors, diuretics) How ACE Inhibitors and ARBs cause prerenal AKI Angiotensin II constricts the efferent arteriole, which increases the glomerular filtration rate. When angiotensin II levels are low, the efferent arteriole dilates, which decreases GFR How NSAIDs can cause prerenal AKI Blocks prostaglandins that dilates afferent arteriole decreasing GFR Intrarenal AKI Damaged Glomerulus (e.g., glomerulonephritis) Damaged Tubular Cells (e.g., acute tubular necrosis) Intrarenal AKI Prolonged Ischemia Toxic substances (drugs, x-ray contrast dye) Nephrotoxic Drugs - Intrarenal AKI NSAIDs especially indomethacin (interferes with prostaglandin’s protective mechanism) Antibiotics: amphotericin B, aminoglycosides, vancomycin Calcineurin inhibitors: Tacrolimus and cyclosporine Antivirals: Acyclovir Postrenal AKI Prostatic hypertrophy Pelvic masses Nephrolithiasis Hypertension and Diabetes Mellitus are the 2 most common causes. Chronic Kidney Disease Chronic Kidney Disease Chronic Kidney Disease – Metabolic Acidosis Chronic Kidney Disease Secondary hyperparathyroidism

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