Acute and Chronic Renal Failure

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Presentation transcript:

Acute and Chronic Renal Failure Niazy B Hussam Aldin

INTRODUCTION TO ACUTE RENAL FAILURE or injury acute kidney failure is the rapid loss your kidneys' ability to remove waste and help balance fluids and electrolytes in your body. In this case, rapid means less than 2 days. And it may progress to end stage renal disease, uremic syndrome, and death without treatment.  In most cases ARF is usually asymptomatic and is diagnosed when screening of hospitalized patients reveals a recent increase in serum blood urea nitrogen and creatinine. Recent Research's-  The term acute renal failure (AKI) has largely replaced acute renal failure (ARF), reflecting the recognition that smaller decrements in kidney function that do not result in overt organ failure. The term ARF is now reserved for severe AKI, usually implying the need for renal replacement therapy.

Electrolyte Abnormalities Excretion of Na+ is initially increased, probably due to natriuretic factors As glomerular filtration rate (GFR) falls, FeNa rises Maintain volume until GFR <10-20mL/min, then edema Renal failure with nephrotic syndrome, early edema Cannot conserve Na+ when GFR <25mL/min, and FeNa rises with falling GFR 3. Tubular K+ secretion is decreased Aldosterone mediated. Also increased fecal loss of K+ (up to 50% of K ingested) Cannot handle bolus K+, avoid drugs high K+ Do not use K+ sparing diuretics

Bone Metabolism ↓GFR leads to ↑ phosphate ↓ calcium + acidosis In addition,↑ tubular resorption Ca+ ↑ hypocalcemia Other defects include acidosis and decreased dihydroxy-vitamin D production Bone acts as a buffer for acidosis, leading to chronic bone loss in renal failure Low vitamin D causes poor calcium absorbtion and hyperparathyroidism (high PTH) Increased PTH maintains normal serum Ca2+ and PO42- until GFR <30mL/min Chronic hyperparathyroidism and bone buffering of acids leads to severe osteoporosis

Other abnormalities Slight hypermagnesemia with inability to excrete high magnesium loads Uric acid retention occurs with GFR <40mL/min Vitamin D conversion to dihydroxy-Vitamin D is severely decreased Erythropoietin (EPO) levels fall and anemia develops Accumulation of normally excreted substances, "uremic toxins", MW 300-5000 daltons

Associated Problems and Treatment Immunosuppression Patients with CRF, even pre-dialysis, are at increased risk for infection Cell mediated immunity is particularly impaired Hemodialysis seems to increase immunocompromise Complement system is activated during hemodialysis Patients with CRF should be vaccinated aggressively

Hypertension Blood pressure control is very important to slowing progression of renal failure About 30% of end-stage renal disease (ESRD) is related to hypertension Overall risk of CRF with creatinine >2.0mg/dL is ~2X in five years with HTN Patients with grade IV (severe) HTN have 22X increased risk vs. normal for CRF Targetted mean pressure 92-98mm Hg in patients with renal failure and proteinuria Patients with HTN and albuminuria >1gm/day, blacks, diabetics have higher ESRD risk

Note- All cases of both chapter 17and 18 are included