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acute renal failure (ARF)

introduction

  • ARF is a common finding in the ED patient and one of the clinician's tasks is to decide on whether it is pre-renal, renal or post-renal.
  • exclusion of urinary retention by checking with a bladder scanner is a simple first step
  • patients in clinical the shocked hypotensive patient will obviously need this addressed ASAP.

investigations to help determine pre-renal vs post-renal causes

index pre-renal ARF renal ARF
blood urea : creatinine ratio (in mM) >40:1 < 40:1
specific gravity urine >1.013 <1.013
urinary sodium concentration (mM) <10>10
urine osmolality >500 <350
urine:plasma osmolar ratio >1.2<1.2
Fe Na % <1>3
renal failure index<1>4
  • fractional excretion of sodium (Fe Na %):
    • = [(UNa / PNa) / (UCr / PCr)]x100
    • this reflects the fraction of filtered sodium that escapes reabsorption & is excreted in urine
    • note that urine & plasma levels of sodium & creatinine must be taken simultaneously
  • renal failure index (RFI)
  • urinary sodium indices
    • urinary sodium concentration provides information on the integrity of tubular reabsorptive function
    • normally urimary sodium concentration parallels sodium intake
    • low urinary sodium thus indicates not only intact tubular reabsoptive mechanism but also the presence of a stimulus to conserve sodium
    • urinary sodium concentration (and fractional excretion of sodium (FENa)) helps distinguish between the two most common causes of ARF: pre-renal azotaemia and ATN.
    • urinary indices are most helpful in oliguric patients. In euvolaemic individuals who are in sodium balance, & who have a normal sodium intake and normal renal function will have urinary sodium concentration < 20mEq/L & FENa < 1%
    • UNa < 20mEq/L, FENa < 1%
      • normal individuals
      • oliguric pts:
        • pre-renal azotaemia
        • acute glomerulonephritis (check urine microscopy for red cell casts)
        • acute obstruction
        • some cases of contrast-induced ATN
        • some cases of rhabdomyolysis-associated ATN
        • early sepsis
        • 10% of cases of oliguric ATN
    • UNa 20-40mEq/L:
      • non-discriminatory as may be either pre-renal, mild ATN or diuretic use, etc
    • UNa > 40mEq/L, FENa > 1%
      • 90% of cases of ATN
      • chronic obstruction
      • diuretic drugs
      • osmotic diuresis
      • underlying chronic renal failure

pre-renal causes of ARF

general features

  • usually have:
    • BUN:CRN ratio (in mM) > 100
    • FE Na < 1% & urinary sodium < 20 mEq/dL
  • if it is severe & prolonged, may result in ATN
  • NB. “renal dose” dopamine does not effect clinical outcomes in pts with ARF (Ann Int Med April 2005)

aetiology

volume loss:

  • GIT: vomiting, diarrhoea, NG drainage
  • renal: diuresis
  • blood loss
  • insensible losses
  • third space sequestration
  • pancreatitis
  • peritonitis
  • trauma
  • burns

cardiac:

  • AMI, valvular disease, cardiomyopathy
  • decreased effective arterial volume:
    • antihypertensive drugs
    • nitrates

"neurogenic":

  • sepsis
  • anaphylactic
  • hypoalbuminaemia
    • nephrotic syndrome
    • liver disease

impaired intrarenal blood flow:

  • ACE inhibitors
  • NSAIDs (generally reversible):
    • inhibit the normal renal vasodilator PG's which are critical in maintaining glomerular perfusion in pts with diminished renal blood flow such as:
      • elevated renin/AGII levels as in CCF, CRF & cirrhosis
      • elderly, diuretic use, renovascular disease, diabetes

renal causes of ARF

vascular:

  • large vessel:
    • renal artery thrombosis or stenosis:
      • Hx of AF/recent AMI; AAA; N/V/flank pain;­LDH; renal arteriogram;
    • renal vein thrombosis:
      • evidence of nephrotic synd. or PE; flank pain; haematuria; IVCgram;
    • atheroembolic disease:
      • usually age>50;recent aortic procedure;retinal plaques;s/c nodules;palpable purpura; livedo reticularis; vasculopathy; HT; eosinophilia; hypocomplementaemia; skin Bx; renal Bx
  • small & medium vessel:
    • scleroderma
    • malignant HT:
      • severe HT with headaches, cardiac failure, retinopathy, CNS dysfn, papilloedema
      • RBC casts; LVH on ECG with resolution on control of BP
    • HUS, TTP:
      • compatible clinical Hx - diarrhoea; cyclosporin; anovulants;
      • fever, pallor, ecchymoses, neurological abnormalities
      • anaemia, thrombocytopenia, schistocytes, ­LDH, renal Bx

glomerular

  • systemic diseases:
    • SLE, infective endocarditis, systemic vasculitis (PAN, Wegener's), HSP, cryoglobulinaemia
    • Goodpasture's syndrome
  • primary renal disease:
    • post-strept. & other post-infectious GN
    • rapidly progressive GN

tubulointerstitial:

  • infections: acute bilateral pyelonephritis
  • allergic interstitial nephritis:
    • recent ingestion of drug - b lactams, NSAIDs, diuretics, proton pump inhibitors, sulphonamides, allopurinol, rifampicin
    • LOW, malaise, fever, rash or arthralgias
    • classic triad uncommon: fever, rash and eosinophilia
    • WBC casts (often eosinophils); RBCs; proteinuria (occas. nephrotic)
    • eosinophilia; skin Bx of rash (leukocytoclastic vasculitis); 
    • renal Bx - mononuclear infiltrates of lymphocytes, plasma cells & eosinophils +/- histiocytes
  • drugs/toxins (many):
    • heavy metals, ethylene glycol, etc
  • multiple myeloma:
    • bone pain; dipstick neg. proteinuria; circ. or urinary paraprotein;
  • acute tubular necrosis (ATN)
    • ischaemia:
      • shock
      • sepsis
      • all causes of severe pre-renal azotaemia
    • nephrotoxins:
      • the fungal mycotoxin, Ochratoxin A (OTA), a secondary metabolite produced by several fungal species, in particular from Aspergillus ochraceus and Penicillium verrucosum which may contaminate foods such as cereals
    • pigments:
    • crystals:
      • uric acid:
        • tumour lysis (chemotherapy); urate crystals on micro.;
      • oxalate:
        • ethylene glycol ingestion; oxalate crystals on micro; tox. screen; acidosis; osmolal gap;

post-renal causes of ARF

  • in the absence of infection, full renal recovery from post-renal ARF is said to be possible even after 1-2 weeks full obstruction, although serum CRN may not return to baseline for several weeks
  • as the onset of irreversible loss of renal function with obstruction appears to be gradual, a few days delay in diagnosis generally is considered acceptable, although common sense dictates that obstructions should be detected and relieved as expeditiously as possible.

intrarenal & ureteral:

  • kidney stone
  • sloughed papilla (esp. if sudden deterioration of renal fn in diabetes, analgesic nephropathy or HbS)
  • malignancy
  • retroperitoneal fibrosis
  • crystal precipitation - uric acid (eg. with tumour lysis), oxalic acid, sulphonamide
  • methotrexate, aciclovir or Bence Jones protein precipitation
  • surgical misadventure

bladder:

  • acute urinary retention
  • chronic urinary retention
  • kidney stone
  • blood clot
  • prostatic hypertrophy
  • bladder carcinoma
  • neurogenic bladder

urethra:

  • phimosis
  • stricture

clinical features and complications of ARF

cardiovascular:

metabolic:

neurologic:

  • asterixis
  • NM irritability
  • mental state changes
  • somnolence
  • coma

GIT:

  • nausea, vomiting
  • gastritis
  • GIT bleeding
  • malnutrition

haematologic

infectious:

arf.txt · Last modified: 2020/01/07 21:15 (external edit)