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Kidney (Acute Renal Failure/Acute Kidney Injury) (What: Increase in serum…

- - - - HOW
        
        Non-selective COX inhibitor (inhibit COX 1 and COX 2 inhibiting prostaglandin synthesis and hence reduce inflammation): Naproxen
        
        Selective COX-2 inhibitor: Rofecoxib which reduces risk of peptic ulcer compared to non-selective inhibitor but this drug increases risk of stroke and heart attack/Celecoxib
        
        Both below can lead to AKI. But selective COX-2 also decreases renal clearance.
        
        PG is increased in prolonged renal vasoconstriction such as chronic kidney disease (esp stage 3 or worse, GFR <60ml/min/1.73m2), volume depletion from diuresis, vomiting, diarrhea, effective arterial volume depletion frm heart failure, nephrotic syndrome or cirrhosis, older age and severe hypercalcemia with associated renal arteriolar vasoconstriction. This serves to protect the glomerular filtration rate via inducing renal arteriolar vasodilation decreasing preglomerular resistance.
        NSAID-induced inhibition of PG-mediated afferent vasodilation and reduction in peritubular blood flow may also increase the risk of ischemic acute tubular necrosis (ATN) or other nephrotoxin-induced tubular injury from drugs such as aminoglycosides, amphotericin B, hydroxyethyl starch, and radiocontrast material
        
        Detected via raised serum creatinine within 3-7 days of therapy
        
        Urinalysis is usually negative for hematuria and proteinuria. Although low-level proteinuria (<500 mg/day) may be observed, significant proteinuria (ie, >1 g/day) is uncommon and suggests an NSAID-induced glomerular lesion (minimal change disease or membranous nephropathy) rather than hemodynamically mediated AKI.
        The urine sediment may contain hyaline casts and, if acute tubular necrosis (ATN) has developed, renal tubular epithelial cell casts, renal tubular epithelial cells, or granular casts. White blood cells (WBCs) and WBC casts are not seen in hemodynamically mediated AKI and suggest acute interstitial nephritis (AIN).
    - - Reduce GFR, more marked with bilateral renal artery stenosis, hypertensive nephrosclerosis, heart failure, polycystic kidney disease, or chronic kidney disease where intrarenal perfusion pressure may already be reduced, a setting in which maintenance of GFR is maintained in part by an angiotensin II-induced increase in resistance at the efferent (postglomerular) arteriole. Blocking this response with an ACE inhibitor will sequentially relax the efferent arteriole, lower intraglomerular pressure, and reduce the GFR. Patients with acute volume loss due to vomiting and/or diarrhea may be particularly susceptible.
        Detected via rise in the serum creatinine concentration three to five days
        
        Termination of the ACE inhibitor should be considered if hyperkalemia cannot be controlled or the serum creatinine concentration increases more than 30 percent above the baseline value within the first six to eight weeks when blood pressure is reduced.
      - Hyperkalemia( serum potassium concentration above 5.5 meq/L) — ACE inhibitor will decrease angiotensin 2 which will reduce aldosterone secretion, thereby impairing the efficiency of urinary potassium excretion.
        
        More marked in:
        a) Renal insufficiency
        b) Diabetes,
        c) Concurrent use of a drug promoting potassium retention such as a potassium-sparing diuretic or a nonsteroidal anti-inflammatory drug, or among the elderly
        d) Heart failure (decreased renal perfusion due to the fall in cardiac output and, often, combined therapy with a mineralocorticoid receptor antagonist (spironolactone or eplerenone) )
    - - Quick recap of RAAS: Decrease in perfusion of renal juxtaglomerular apparatus leads to activation of RAAS system. Renin is secreted by juxtaglomerular apparatus which cleaves angiotensinogen produced by the liver into angiotensin 1 which is converted by angiotensin converting enzyme (surface of pulmonary and renal endothelium) into angiotensin 2.
        
        Sympathetic activity
        
        Stimulates adrenal cortex to secrete aldosterone which #
        
        Tubular Na and Cl reabsorption and increase K secretion, H20 retention
        
        Arteriolar vasoconstriction increase blood pressure
        
        Stimulate posterior pituitary gland to secrete ADH which increase water absorption at collecting duct
        
        ACE Inhibitor inhibit conversion of angiotensin 1 to angiotensin 2. eg captopril
        ARB prevent angiotensin 2 from binding to receptors eg losartan
        Renin inhibitor eg aliskiren
- - - - Thrombotic microangiopathy, malignant hypertension, scleroderma, antiphospholipid syndrome, preeclampsia
    - - Radiocontrast, aminoglycosides, cisplatin
        
        Cisplatin: Interferes with DNA replication hence kills the cells that proliferates quickly. Side effects include nephrotoxicity, neurotoxicity, N/V, Ototoxicity, hemolytic anemia, Hypomag/kal/calcemia
      - Hypotension or shock, prolonged prerenal azotemia, postoperative sepsis syndrome, rhadomyolysis, hemolysis, drugs)