Acute Renal Failure.ppt
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Acute Renal Failure
MDRDeGFR= 186 x Screat X Age X 1.21 [if black] X o.74 [if female] Undersetimates GFR in healthy people (when GFR >60 ml/min)
Cockcroft-Gault formula(140-Age) X Mass (In KG) X [o.85 if female]/72 X Serum Creat
The non-steady-state conditions that prevail in ARF preclude estimation of GFR using standard formulae derived from patients with chronic kidney disease.
RR= 2.4RR= 4.15RR=6.37
- ShortcomingsThe assignement of corresponding changes in serum creat and changes in urine output to the same strata is not based on evidence. The criteria that results in the least favorable rifle strata to be used.The patient would progress from "risk" on day one to "injury" on day two and "failure" on day three, even though the actual GFR has been
Diagnostic criteriaAbrupt (within 48 hours) absolute increase in the serum creatinine concentration of 0.3 mg/dL (26.4 micromol/L) from baseline.
Or a percentage increase in the serum creatinine concentration of 50 percent.
Or oliguria of less than 0.5 mL/kg per hour for more than six hours. The diagnostic criteria could be applied only after volume status had been optimized Urinary tract obstruction needed to be excluded if oliguria was used as the sole diagnostic criteria
Syndromes of acute renal failurePrerenal ARFIntravascular volume depletionDecreased effective blood volumeAltered intrarenal hemodynamicspreglomerular (afferent) vasoconstrictionpostglomerular (efferent) vasodilationIntrinsic ARFAcute tubular necrosisischemicnephrotoxicacute interstitial nephritisacute glomerulonephritisacute vascular syndromesPostrenal ARF
Epidemiology of ARF
The observed incidence, etiology, and outcomes of ARF are highly dependent upon the populations studied and the definition of ARF employed.
The absence of centralized registries to track the incidence and outcomes of patients with ARF has hindered our understanding of its epidemiology.
NATURE CLINICAL PRACTICE NEPHROLOGY (2006) 2,364-377The changing epidemiology of acute renal failure
Key Points The absolute incidence of acute renal failure (ARF) has increased in the past two decades, while the mortality rate has remained relatively staticThe lack of a standard definition of ARF complicates the process of identifying the factors that underlie changes in epidemiology of this condition.Despite the use of different definitions in different studies, various factors that have contributed to altered epidemiology of ARF in the past few decades have been identifiedThese factors include geographical site of disease onset (developed vs developing countries; community vs hospital vs intensive care unit), patient age, infections (HIV, malaria, leptospirosis and hantavirus), concomitant illnesses (cardiopulmonary failure, hematooncological disease), and interventions (hematopoietic progenitor cell and solid organ transplantation)
Prerenal Acute Renal Failure
GFR is reduced as a result of hemodynamic disturbances that decrease glomerular perfusion.
The defining feature of prerenal ARF is the absence of cellular injury and the normalization of renal function with reversal of the altered hemodynamic factors.
OF PRERENAL ARFPathophsiology
Diagnosis of Prerenal ARFHxP/EUrine sediment (usually normal, without cellular elements or abnormal casts, unless chronic kidney disease is present)UNa< 15 meq/L (>20 in ATN)U/Pcreat> 20 (
BUN/CREAT of >20 is typical, BUT is not specific to prerenal ARF and may also be seen:Obstructive uropathyGastrointestinal bleeding Other states associated with increased urea production.
FE UreaPatients on diureticsPrerenal azotemia due to vomiting on NG suctioning.FE Na may be low is sepsis, RCN, myoglobinuria, nonoliguric ATN, acute GN, urinary tract obstruction and renal allograft rejection
Significance of the fractional excretion of urea in thedifferential diagnosis of acute renal failure
102 patients were divided into three groups:Prerenal azotemia (N 50)Prerenal azotemia treated with diuretics (N 27)ATN (N 25)
Kidney International, Vol. 62 (2002), pp. 22232229
- FENa was low only in the patients with untreated plain prerenal azotemia while it was high in both the prerenal with diuretics and the ATN groups. FEUN was essentially identical in the two pre-renal groups (27.9 2.4% vs. 24.5 2.3%), and very different from the FEUN found in ATN (58.6 3.6%, P < 0.0001).92% of the patients with prerenal azotemia had FENa
Low FE urea
ARF Associated with ACE Inhibitors and Angiotensin Receptor Blockers
Acute renal failure can develop acutely, when ACEI or ARB therapy is initiated, or in patients receiving chronic therapy, especially in patients with underlying CHF
Predisposing factors:Advanced cardiac failure with low mean arterial pressureVolume depletion due to diuretic therapyThe presence of renal vascular diseaseThe concomitant use agents with vasoconstrictor effects (NSAIDs, cyclooxygenase-2 inhibitors, cyclosporine, and tacrolimus) CKD: The risk of ARF is higher in patients with chronic kidney disease of any cause than in patients with normal renal function
Serum creatinine and electrolyte concentrations should be measured before and 1 wk after initiating or changing the dose of therapy
An increase in serum creatinine of >0.5 mg/dl if the initial serum creatinine is 1.0 mg/dl if the baseline serum creatinine is >2.0 mg/dl, has been suggested as a threshold for discontinuation of therapy
The development of ARF should prompt an evaluation for cardiac failure, hypotension, volume depletion, use of a concomitant vasoconstrictive agent, or renovascular disease.
Acute Renal Failure Associated with NSAIDS
Nonsteroidal anti-inflammatory drugs (NSAID) agents inhibit the synthesis of vasodilatory prostaglandins in the kidney.
Severe CHFAdvanced liver diseaseSevere atherosclerotic vascular diseaseCKD
Elderly patients are at increased risk due to the increased prevalence of cardiac dysfunction, occult renal vascular disease, and subclinical chronic kidney disease.
Abdominal Compartment Syndrome
Unusual cause of decreased renal perfusion associated with increased intra-abdominal pressure
Trauma patients who require massive volume resuscitationMechanical limitations of the abdominal wall (tight surgical closures or scarring after burn injuries) Medical etiologies that are characterized by intraabdominal inflammation with fluid sequestration, such as bowel obstruction, pancreatitis, and peritonitis.
Clinical manifestationsRespiratory compromise Decreased cardiac output Intestinal ischemia Hepatic dysfunction Oliguric renal failure
The renal insufficiency results from decreased renal perfusion and correlates with the severity of the increased intraabdominal pressure.
Oliguria develops when the intraabdominal pressure exceeds 15 mmHg, with anuria developing at pressures >30 mmHg.
DiagnosisThe diagnosis should be suspected in patients with a tensely distended abdomen and progressive oliguria.
Measurement of intraabdominal bladder pressure.
Abdominal compartment syndrome can be excluded when the bladder pressure is 25 mmHg.
Treatment Abdominal decompression:Paracentesis if massive ascites.Surgical decompression is required in the majority of patients.Renal failure usually recovers promptly after relief of the increased intraabdominal pressure
Postrenal Acute Renal Failure
Intrinsic ExtrinsicLower tract obstruction
Urine output?The obstruction: Complete Anuria
Pathophysiology After the acute onset of obstruction, GFR declines progressively, but it does not fall to zero.
Factors that maintain GFR include continued salt and water reabsorption along the nephron, dilatation of the collecting system, and alterations in renal hemodynamics.
Intratubular pressure rises acutely, but it begins to decline within the first 4 to 8 h, returning to nearly normal by 24 h.
Ureteral Pr RBF GFR 1- 2 H 2-5 H Late phase
Complete obstructionRecovery after relief of obstruction depends on:Severity Duration Less than 1 wk duration, recovery complete. Little or no recovery after 12 wk.
Partial obstructionThe course after relief of partial obstruction is less predictableDepends on Severity DurationPresence of infection or preexisting renal disease.
Relief of obstruction may be accompanied by a post-obstructive diuresis;Excretion of salt and water retained during the obstruction.Persistent salt-wasting and impaired urinary concentrating ability .
DiagnosisElderly male patientsMeasurement of a post-voiding residual bladder volume, either by an bedside ultrasound bladder scan or by placement of an indwelling bladder catheter.
DiagnosisUltrasonography Sensitivity and specificity are highNon diagnostic Early in the course of postrenal ARF.Severe volume depletion.Obstruction is due to retroperitoneal disease (e.g., retroperitoneal fibrosis, tumors, adenopathy) encasing the ureter and preventing dilatation
Non-contrasted CT scanning may be particularly useful for the identification of obstructing kidney stones
Etiology of Intrinsic ARF