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Acute Kidney Injury

Acute Kidney Injury. - Rapid decline in renal filtration function. Acute Kidney Injury. Prerenal AKI. Most common form of AKI 2 major causes: Hypovolemia Renal fluid loss Decreased intake of fluids Altered renal hemodynamics resulting in hypoperfusion

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Acute Kidney Injury

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  1. Acute Kidney Injury - Rapid decline in renal filtration function

  2. Acute Kidney Injury

  3. Prerenal AKI • Most common form of AKI • 2 major causes: • Hypovolemia • Renal fluid loss • Decreased intake of fluids • Altered renal hemodynamics resulting in hypoperfusion • Low cardiac output state due to pulmonary hpn leading to left heart failure • Systemic vasodilation due to antihypertensives

  4. Acute Kidney Injury

  5. Intrinsic AKI • Major causes: • Renovasculat Obstruction • Diseases of the Glomeruli or vasculature • Acute Tubular necrosis • Ischemia • Infection, with or without sepsis • Toxins: exogenous, endogenous • Interstitial Nephritis • Allergic • Infection • Inflammatory, nonvascular • Intratubular obstruction

  6. ACUTE KIDNEY INJURY • Tubulointerstitial disease - acute interstitial nephritis • Due to baterial, viral and other miscellaneous infection • Streptococcus, staphylococcus, legionella, salmonella, Brucella, yersinia • Interstitial edema with cortical and medullary infiltration by mononuclear cells and polymorphonuclear leukocytes and patchy areas of tubule cell necrosis

  7. Chronic form: fibrosis, predominance of mononuclear, widespread atrophy, luminal dilatation and thickening of the tubule basement membranes • Defects in renal function • Proximal tubule dysfunction • Selective reabsorptive defects • hypokalemia, • Aminoaciduria • Glycoasuria • Phosphaturia • Uricosuria • Bicarbonaturia

  8. Defects in urinary acidification and concentrating ability • Hyperchloremic metabolic acidosis • Maximal Urine pH <5.3 • Caused by reduced capacity to generate and excrete ammonia due to reduction in renal mass

  9. Functional consequences of tubulointerstitial disease

  10. Modifiers influencing the progression of renal diseases • Risk factors for progressive loss of renal function • Systemic HPN • Diabetes • Activation of RAAS system

  11. Poor cho control will aggrevate renal progression in both diabetic and non diabetics • Angiotensin II produces intraglomerular HPN and stimulate fibrogenesis • Aldosterone • Serves as an indeoendent fibrogenic mediator of progression loss apart from its role in modulating Na and K homeostasis

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