Click here to load reader

ACUTE & CHRONIC KIDNEY FAILURE

  • View
    60

  • Download
    9

Embed Size (px)

DESCRIPTION

ACUTE & CHRONIC KIDNEY FAILURE. By Maritza I. Garcia-Duran & Joao Mc-O’neil Internal Medicine 06/21/2010. ACUTE KINEY FAILURE a.k.a. Acute Kidney Injury (AKI). rapid loss of kidney function REVERSIBLE. CAUSES. Other Signs and Symptoms of AKI. - PowerPoint PPT Presentation

Text of ACUTE & CHRONIC KIDNEY FAILURE

  • ACUTE & CHRONIC KIDNEY FAILUREBy Maritza I. Garcia-Duran & Joao Mc-OneilInternal Medicine06/21/2010

  • ACUTE KINEY FAILURE A.K.A. ACUTE KIDNEY INJURY (AKI)rapid loss of kidney function

    REVERSIBLE

  • CAUSES

  • OTHER SIGNS AND SYMPTOMS OF AKIf/b generalized swelling, d/t waste products build in the blood.Met. AcidosisArrhythmias d/t hyperkalemia. Including v-tach and v-fibEncephalopathy = altered thinking and pericarditis d/t uremia and low serum calciumAnemia d/t decreased EPO productionHypertension d/t inc fluid deposited in lung causing CHFTachypnea

  • DIAGNOSISRapid time course (less than 48 hours)Reduction of kidney function Rise in serum creatinine Absolute increase in serum creatinine of 0.3mg/dlPercentage increase in serum creatinine of 50%Reduction in urine output, defined as
  • HUMAN REFERENCE RANGE OF SERUM CREATININE0.5 to 1.0mg/dL (about 45-90 mol/L) for women0.7 to 1.2mg/dL (60-110 mol/L) for men. While a baseline serum creatinine of 2.0mg/dL (150 mol/L) may indicate normal kidney function in a male body builder, a serum creatinine of 1.2mg/dL (110 mol/L) can indicate significant renal disease in an elderly female

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

  • 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 furosemideRenal replacement therapy: like hemodialysis

  • COMPLICATIONSMetabolic acidosisHyperkalemiapulmonary edemaend-stage renal failure requiring lifelong dialysis or a kidney transplant.

  • QUESTIONFor each of the following questions, choose the pathophysiologic mechanism of reduced glomerular filtration rate (GFR).Acute tubular necrosisDecreased relaxation of afferent arteriolesGlomerulonephritisHypovolemiaIncreased relaxation of efferent arterioles

  • QUESTION 1A 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 patients 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

  • ANSWER E: INCREASED RELAXATION OF THE EFFERENT ARTERIOLESDecreased 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.

  • QUESTION 2An 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.

  • ANSWER: D , HYPOVOLEMIAClassic 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.

  • CHRONIC KIDNEY DISEASE (CKD), ALSO KNOWN AS CHRONIC RENAL DISEASE

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

    IRREVERSIBLE

  • Causesdiabetic nephropathy, hypertension glomerulonephritis.HIV nephropathy.PCKD

  • CLASSIFICATION Vascular-renal artery stenosis -ischemic nephropathy, hemolytic-uremic syndrome and vasculitisGlomerular-focal segmental glomerulosclerosis and IgA nephritisdiabetic nephropathy and lupus nephritisTubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathyObstructive such as with bilateral kidney stones and diseases of the prostateOn rare cases, pin worms infecting the kidney can also cause idiopathic nephropathy.

  • Signs and symptomsincrease in serum creatinine or protein in the urinehypertension and/or suffering from congestive heart failureUrea 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").

  • Hyperkalemia : symptoms malaise and potentially fatal cardiac arrhythmiasErythropoietin decreased = anemia, which causes fatigueFluid volume overload - mild edema to life-threatening pulmonary edemaHyperphosphatemia - due to reduced phosphate excretionhypocalcemia (due to vitamin D3 deficiency)- tetany.--progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function.

  • 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 atherosclerosisCardiovascular disease-worse prognosis

  • DIAGNOSISIt 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 PCKDnuclear medicine MAG3 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.

  • PCKD-CKD

  • TREATMENTThere 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]

  • 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 5erythropoietin 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.TREATMENT

  • QUESTION #1A 57 yearold man is on maintenance hemodialysis for chronic renal failure. Which of the following metabolic derangement can be anticipatedHypercalcemiaHypophosphatemiaOsteomalaciaVitamin D excessHypoparathyroidism

  • ANSWERC. OsteomalaciaChronic 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 osteitis fribrosa cystica may all be seen. (Kasper et al., 2005, pp. 1656-1657).

  • QUESTION #2A 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.GentamicinErythromycinNafcillinChoramphenicol.

  • ANSWERB. GentamicinMany 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 isoxazolyl penicillins (nafcilllin and oxacillin) and moxifloxacin. (Kasper et al., 2005, p. 1662, 19).

  • What is man but an ingenious machine designed to turn with infinite artfulness, the red wine of shiraz into urine !

    Isak Denison

    **