Acute renal failure ARF

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1 Acute renal failure ARF

2 Definition ARF is a clinical syndrome characterized by an abrupt decline in GFR and the accumulation of nitrogenous waste (BUN & creatinine). The decrease in GFR occurs relatively rapidly, over the course of days to weeks. (By contrast, CRF develops over months or years.)

3 Epidemiology of acute renal failure Common clinical syndrome broad aetiological profile 5 % of hospital admissions, 30 % of admissions to ICU.

4 Etiology prerenal (about 75 %), intrinsic or parenchymal renal disease (25 %), postrenal (5 %)

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9 Clinical approach to the diagnosis Is it ARF or acute-on-chronic renal failure? Is there renal tract obstruction? Is there reduction in effective ECF volume? Has there been a major vascular occlusion? Is there parenchymal renal disease other than ATN?

10 Is the renal failure really acute? Differential diagnosis Acute renal failure normal or enlarged kidneys no/mild anemia (BUT HUS) Ca & P normal Chronic renal failure smaller kidneys severe anemia without serious symptomes nocturia, pruritus, long lasting HT, neuropathy Ca, P, abnormal biochemical values / patient without serious symptomes

11 Urine volume oliguria < 400 ml/day anuria < 50 ml/day Serum chemistry BUN (back-diffusion depends on urine flow rate) creatinine

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14 Treatment of ARF

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18 Prerenal ARF Glomerular perfusion GFR absence of any structural abnormality of the renal parenchyma rapidly and completely reversed RBF sufficient to sustain the viability of renal tubular cells ( ATN)

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21 Acute tubular necrosis (ATN) Renal parenchymal injury caused by ischemia or exposure to nephrotoxins, which particularly injure the tubular epithelium. Ischemic nephrotoxins endogenous (e.g. myoglobin, light chains) exogenous (e.g. drugs, heavy metals)

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25 Causes of acute interstitial nephritis (AIN) 1. Drug-related AIN 2. Infection-related AIN 3. Systemic diseases lupus erythematosus Sarcoidosis Sjögren s syndrome 4. Malignancy 5. Idiopathic AIN

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27 CHRONIC RENAL FAILURE

28 Diabetes: The Most Common Cause of ESRD Primary Diagnosis for Patients Who Start Dialysis Other Diabetes 50% 10% Glomerulonephritis 13% Hypertension 27% No. of Dialysis Patients (thousands) Patients (n) Projection 95% CI 243, , ,240 r 2 = 99.8% United States Renal Data System. USRDS 2000 Annual Data Report. June 2000.

29 CHRONIC RENAL FAILURE The progression of chronic kidney disease Uremia clinical abnormalities Renal anemia and renal osteodystrophy Renal replacement therapy

30 Risk Factors for Renal Disease Progression Proteinuria > 1.5 g/24 hr Hypertension Type of underlying renal disease African-American race Male sex Obesity Diabetes mellitus Hyperlipidemia Smoking High protein diet Phosphate retention Metabolic acidosis

31 The epidemiology of CKD USA: 11 % of the population, around 20 million people have CKD

32 Treatment of Renal Disease Progression Goals: stop or slow the rate of GFR decline prevent additional kidney damage cused by superimposed events maintain nutritional status and prevent complications of the uremic syndrome.

33 Slowing the progresion of chronic kidney disease Tight blood pressure control (BP 130/80 mm Hg) using: low sodium diet ACE inhibitors angiotensin receptor antagonists diuretics calcium channel blockers + Dietary protein restriction (0.8-1 g/kg body weight) Glycemic control Decreasing proteinuria

34 CHRONIC RENAL FAILURE The progression of chronic kidney disease Uremia clinical abnormalities Renal anemia and renal osteodystrophy Renal replacement therapy

35 Uremic toxins Low molecular mass solutes: Da urea, creatinine Middle molecules: Da PTH, ß2-microglobulin Large solutes: more than Da myoglobin

36 Major Clinical Abnormalities in Uremia I. Water and electrolyte abnormalities: volume expansion hyperkalaemia metabolic acidosis hyperphosphatemia and hypercalaemia Cardiovascular abnormalities: hypertension congestive heart failure cardiomiopathy pericarditis accelerated atherosclerosis arrhythmias

37 Major Clinical Abnormalities in Uremia II. Gastrointestinal abnormalities: anorexia, nausea, and vomiting uremic fetor stomatitis, gastritis peptic ulcer gastrointinal bleeding Hematologic and immunologic abnormalities: anemia bleeding phagocyte inhibition lymphocytopenia increased susceptibily to infection and neoplasia

38 Major Clinical Abnormalities in Uremia III. Neurological abnormalities: malaise headache irritability and sleep disorders muscle cramps tremor seizures stupor and coma peripheral neuropathy restless legs motor weakness

39 Major Clinical Abnormalities in Uremia IV. Endocrine and metabolic abnormalities: hypertriglyceridemia protein malnutrition impaired growth infertility, sexual dysfunction, and amenorrhea renal osteodystrophy secondary hyperparathyreoidism Dermatologic abnormalities: pallor hyperpigmentation pruritus

40 CHRONIC RENAL FAILURE The progression of chronic kidney disease Uremia clinical abnormalities Renal anemia and renal osteodystrophy Renal replacement therapy

41 Renal Anemia Anemia develops early during renal failure and is one of the major causes of malaise and fatigue. It is normocytic and normochromic but may be complicated by iron deficiency due to gastrointestinal bleeding (microcytic) folate deficiency due to dietary restriction (macrocytic) fibrosis of the bone marrow due to hyperparathyroidism.

42 Correction of Anemia Improves cardiac function, central nervous system symptoms, appetite and sexual function. Erythropoietin administration should be started in the predialysis period. Target hemoglobin: g/l. Sufficient iron and folate stores should be maintained!

43 Renal Osteodystrophy Includes all sceletal disorders of patients with renal failure: osteitis fibrosa osteomalacia mixed and adynamic bone lesions dialysis related amyloidosis

44 CHRONIC RENAL FAILURE The progression of chronic kidney disease Uremia clinical abnormalities Renal anemia and renal osteodystrophy Renal replacement therapy

45 Renal Replacement Therapy Hemodialysis Peritoneal dialysis Kidney transplantation

46 Absolute Indications for Initiation of Dialysis Pericarditis Advanced or progressive uraemic encephalopathy or neuropathy Pulmonary edema and fluid overload unresponsive to diuretic measures Hypertension poorly responsive to treatment Hyperkalaemia attributed to ESRD unresponsive to conservative treatment Bleeding diathesis with clinical bleeding attributed to uraemia Persistent nausea Hakim, Advances Nephrol 23: , 1994

47 Relative Indications for Initiation of Dialysis General Anorexia, fatigue, weakness GFR < 20 ml/min in diabetics or GFR = ml/min (other etiologies) Neurological Peripheral neuropathy (often burning dysesthesia) Restless leg syndrome Cardiovascular Peripheral edema unresponsive to diuretics Hakim, Advances Nephrol 1994; 23:

48 Relative Indications for Initiation of Dialysis (continued) Gastrointestinal Anorexia progressing to nausea and vomiting Gastritis, duodenitis, constipation Ascites without liver disease Hematological Anaemia with poor response to erythropoeitin Infections Increased bleeding tendency due to platelet dysfunction Dermatological Persistent and severe itching Hakim, Advances Nephrol 1994; 23:

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50 Principles of dialysers Countercurrent flow of blood (within capillaries) and dialysate (outside of capillaries). Dialysate Outflow Dialysate Inflow Blood Outflow Blood Inflow Solute Transfer across the Capillary Walls

51 Flow Scheme Hemodialysis Dialyser Anticoagulation Blood Pump Fresh Dialysate Blood to the Patient Used Dialysate Blood from the Patient

52 Patient access Standard Arteriovenous (AV) Fistula at the Wrist modified from Man, Zingraff, Jungers, Long-Term Hemodialysis, 1995

53 Patient access Twin Catheters Placed in the Internal Jugular Vein modified from Man, Zingraff, Jungers, Long-Term Hemodialysis, 1995

54 Haemodialysis Standard Therapy: Intermittent HD ca. 3x4-5 5 h / week

55 Peritoneal Dialysis Natural Semipermeable Membrane : Peritoneum The transport of substances via Peritoneum occurs in both directions: i.e. Waste substances from the blood into the solution and buffer substances in the other direction.

56 Principles of Peritoneal Dialysis Small solute movement occurs by diffusion based on the concentration gradient (urea, creatinine, potasssium). Large solute removal occurs by convection: the solute movement is related to fluid removal. The volume of ultrafiltration depends on the concentration of glucose solution (the length of dwell and the peritoneal membrane characteristics).

57 What is CAPD? C ontinuous A mbulatory P eritoneal D ialysis constant dialysis 24 hours a day the patient can walk around while it's happening peritoneal membrane works as a filter

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59 Summary Renal Replacement Therapies Kidney Transplantation Peritoneal dialysis Best outcome Risk for infections, tumours, bone fractures Not all patients are eligible for transplantation Hemodialysis Most frequent modality, highly efficient but intermittent Risk of intradialytic complications Mainly centre treatment Most frequent home dialysis modality, lower efficiency but continuous treatment Risk of infectious complications

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