acute chronic kidney failure n.
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ACUTE & CHRONIC KIDNEY FAILURE

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ACUTE & CHRONIC KIDNEY FAILURE

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  1. ACUTE & CHRONIC KIDNEY FAILURE By Maritza I. Garcia-Duran & Joao Mc-O’neil Internal Medicine 06/21/2010

  2. ACUTE KINEY FAILURE a.k.a. Acute Kidney Injury (AKI) rapid loss of kidney function REVERSIBLE

  3. CAUSES

  4. Other Signs and Symptoms of AKI • f/b generalized swelling, d/t waste products build in the blood. • Met. Acidosis • Arrhythmias d/t hyperkalemia. Including v-tach and v-fib • Encephalopathy = altered thinking and pericarditis d/t uremia and low serum calcium • Anemia d/t decreased EPO production • Hypertension d/t inc fluid deposited in lung causing CHF • Tachypnea

  5. DIAGNOSIS • Rapid time course (less than 48 hours) • Reduction of kidney function • Risein serum creatinine • Absolute increase in serum creatinine of ≥0.3 mg/dl • Percentage increase in serum creatinine of ≥50% • Reductionin urine output, defined as <0.5 ml/kg/hr for more than 6 hours (about 210mL in 6 hours)

  6. HUMAN REFERENCE RANGE OF SERUM CREATININE • 0.5 to 1.0 mg/dL (about 45-90 μmol/L) for women • 0.7 to 1.2 mg/dL (60-110 μmol/L) for men. • While a baseline serum creatinine of 2.0 mg/dL (150 μmol/L) may indicate normal kidney function in a male body builder, a serum creatinine of 1.2 mg/dL (110 μmol/L) can indicate significant renal disease in an elderly female

  7. MANAGEMENT treatment of the underlying cause avoid nephrotoxins (antibiotics, chemotherapeautics, contrast dye, PCN, Aminoglycosides, ACEI, NSAIDS, etc.) Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output urinary catheter: helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate

  8. Specific therapies intravenous fluids is typically the first step to improve renal function. Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. inotropes such as norepinephrine and dobutamine to improve cardiac output and renal perfusion. Dopamine may be harmful. Diuretic agents like furosemide Renal replacement therapy: like hemodialysis

  9. COMPLICATIONS • Metabolic acidosis • Hyperkalemia • pulmonary edema • end-stage renal failure requiring lifelong dialysis or a kidney transplant.

  10. QUESTION • For each of the following questions, choose the pathophysiologic mechanism of reduced glomerular filtration rate (GFR). • Acute tubular necrosis • Decreased relaxation of afferent arterioles • Glomerulonephritis • Hypovolemia • Increased relaxation of efferent arterioles

  11. Question 1 • A 55 yo male has a history of HTN and MI. He is seen in the clinic to follow up on his blood pressure. There are no sxs. The patient’s current medical regimen includes amlodipine, hydrochlorothiazide, and atenolol. Blood pressure is measured at 165/83 in both arms. The remainder of the physical examination is notable for an abdominal bruit. Lisinopril is added to the regimen. One week later blood work shows a creatinine that has risen from 1.3mg/dL to 5.0 mg/KL

  12. Answer E: Increased RELAXATION OF THE EFFERENT ARTERIOLES • Decreased renal perfusion, or pre-renal failure, is a common cause of renal failure and is often rapidly reversible. GFR is manteined at a constant state by PG → relax Afferent arteriole, and Ang II → contract Efferent arteriole (EA). • An ACEI (Lisinopril) → decrease Ang II → increase relaxation of EA → decrease GFR → increase creatinine.

  13. Question 2 • An 88-year-old female is admitted to the hospital after being found in her apartment with altered mental status by family members. Physical examination is notable for delirium, poor skin turgor and dry MM. BUN is 63mg/dL, and creatinine is 1.3 mg/dL.

  14. ANSWER: D , HYPOVOLEMIA • Classic presentation of dehydration with poor skin turgor and dry MM. In light of her advance age, a creatinine of 1.3 mg/dL reflects very poor renal functon.

  15. Chronic kidney disease (CKD), also known as chronic renal disease

  16. progressive loss of renal function over a period of months or years. IRREVERSIBLE

  17. Causes • diabetic nephropathy, • hypertension • glomerulonephritis. • HIV nephropathy. • PCKD

  18. CLASSIFICATION • Vascular-renal artery stenosis -ischemic nephropathy, hemolytic-uremic syndrome and vasculitis • Glomerular-focal segmental glomerulosclerosis and IgA nephritis • diabetic nephropathy and lupus nephritis • Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy • Obstructive such as with bilateral kidney stones and diseases of the prostate • On rare cases, pin worms infecting the kidney can also cause idiopathic nephropathy.

  19. Signs and symptoms • increase in serum creatinine or protein in the urine • hypertension and/or suffering from congestive heart failure • Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). • Urea is excreted by sweating and crystallizes on skin ("uremic frost").

  20. Hyperkalemia : symptoms malaise and potentially fatal cardiac arrhythmias • Erythropoietin decreased = anemia, which causes fatigue • Fluid volume overload - mild edema to life-threatening pulmonary edema • Hyperphosphatemia - due to reduced phosphate excretion • hypocalcemia (due to vitamin D3 deficiency)- tetany.--progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function.

  21. Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia) • accelerated atherosclerosis • Cardiovascular disease-worse prognosis

  22. DIAGNOSIS • It is important to differentiate CKD from acute renal failure (ARF) because ARF can be reversible. • gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). • Abdominal ultrasound CKD KIDNEYS ARE SMALLER THAN NL (LESS THAN 9CM), except in DM nephropathy or PCKD • nuclear medicineMAG3 scan to confirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99.

  23. PCKD-CKD

  24. TREATMENT • There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. • If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. • In more advanced stages, treatments may be required for anemia and bone disease. • Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a • kidney transplant.[1]

  25. TREATMENT • The goal of therapy is to slow down or halt the otherwise relentless progression of CKD to stage 5. • Control of blood pressure (ACEIS, OR ARBs) as they have been found to slow the progression of CKD to stage 5 • erythropoietin and vitamin D3, calcium. • Phosphate • stage 5 CKD, renal replacement therapy is required, in the form of either dialysis or a transplant. • dietary modifications includes limiting protein intake.

  26. QUESTION #1 A 57 yearold man is on maintenance hemodialysis for chronic renal failure. Which of the following metabolic derangement can be anticipated • Hypercalcemia • Hypophosphatemia • Osteomalacia • Vitamin D excess • Hypoparathyroidism

  27. Answer C. Osteomalacia Chronic renal failure treated with hemodialysis results in predictable metabolic abnormalities. The kidneys fail to excrete phosphate, leading to hyperphosphatemia and fail to excrete phosphate, leading to hyperphosphatemia, and fail to syntehsize 1,25 (OH)2D3. Vitamin D deficiency causes impaired interstitial calcium absorption. Phosphate retention, defective intestinal absorption, and skeletal resistance to parathyroid hormone all results in hypocalcemia. Hypocalcemia causes secondary hyperparathyroidism, and the excess PTH production worsens the hyperphosphatemia by increasing phosphorus release from bone. These derangements impair collagen synthesis and maturation, resulting in skeletal abnormalities collectively reffered to as renal osteodystrophy. Osteomalacia, osteosclerosis, and osteitisfribrosacystica may all be seen. (Kasper et al., 2005, pp. 1656-1657).

  28. QUESTION #2 A 60 year old patient with long-standing diabestes has a creatinine of 3.6 which has been stable for several years. Which of the following antibiotics requires the most dosage modification in chronic renal failure? • Tetracycline. • Gentamicin • Erythromycin • Nafcillin • Choramphenicol.

  29. ANSWER B. Gentamicin Many drug require dosage modifications in chronic renal insufficiency. Bioavailability, distribution, action, and elimination of drugs all may altered. Drug that are nephrotoxic may be contraindicated or used only with extreme care in renal insuficiency. The amino-glycosides, vancomycin, ampicillin, most cephalosporins, methicillin, penicillin G, sulfonamides, and trimethoprim all should be given in reduced dosage to patients with chronic renal failure. The aminoglycosides and vancomycin can be nephrotoxic and should be used with caution in renal insufficiency. The small group of antibiotics not needing dosage modification includes chloramphenicol, erythromycin, the isoxazolylpenicillins (nafcilllin and oxacillin) and moxifloxacin. (Kasper et al., 2005, p. 1662, 19).

  30. “What is man but an ingenious machine designed to turn with ‘infinite artfulness’, the red wine of shiraz into urine” …! Isak Denison