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• Low cardiac output state due to pulmonary hpn leading

to left heart failure• Systemic vasodilation due to antihypertensives

Acute Kidney Injury

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

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

– 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

– 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

Functional consequences of tubulointerstitial disease

FUNCTIONAL CONSEQUENCES OF TUBULOINTERSTITIAL DISEASE

DEFECT CAUSE(S)

Reduced glomerular filtration rate Obliteration of microvasculature and obstruction of tubules

Fanconi Syndrome Damage to proximal tubular reabsorption of glucose, amino acids, phosphate, and bicarbonate

Hyperchloremic acidosis 1. Reduced ammonia production2. Inability to acidify the collecting duct fluid (distal

renal tubular acidosis)3. Proximal bicarbonate wasting

Tubular or small-molecular-weight proteinuria

Failure of proximal tubule protein reabsorption

Polyuria, isosthenuria Damage to medullary tubules and vasculature

Hyperkalemia Potassium secretory defects including aldosterone resistance

Salt wasting Distal tubular damage with impaired sodium reabsorption

Modifiers influencing the progression of renal diseases

• Risk factors for progressive loss of renal function– Systemic HPN– Diabetes– Activation of RAAS system

• 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