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renal medicine (nephrology)

  • Help prevent AKI in the ED:
    • withhold ACEIs, ARBs, diuretics, sulfonylureas, metformin, SGLT2 inhibitors in patients with dehydration or hypotension
    • avoid NSAIDs in patients or combined ACEIs/ARBs and diuretics especially if dehydrated
    • avoid NSAIDs or other nephrotoxic drugs such as gentamicin in patients with CKD
    • early Mx of hypovolaemia
    • avoid IV contrast unless necessary
  • as a general rule ALL dialysis patients or renal transplant patients who require admission should FIRST be offered to the renal unit irrespective of reason for admission
  • the following should be strongly considered for referral to a renal clinic if not already managed:
    • acute kidney injury (increase in serum creatinine to ≥1.5 times baseline, or increase in serum creatinine ≥26.5 μmol/l within 48 hours or significantly decreased urine output)
    • acute urine sedimentation / proteinuria
    • chronic renal impairment with eGFR < 30
  • early detection of chronic kidney disease:
    • eGFR and urine ACR every 1-2 yrs if normal but risk factors such as diabetes or hypertension
    • if elevated urine ACR:
      • repeat twice in next 3 months with first morning void specimens
    • if eGFR < 60:
      • repeat within 1 week and if stable, rpt twice within 3 months
        • if falls by 20% or more - possible AKI - consult nephrologist
    • yellow phase CKD:
      • eGFR 45-59 or,
      • eGFR >60 with microalbuminuria (urine ACR males 2.5-25 or females 3.5-35mg/mmol)
      • see yellow action plan:
        • Ix to find cause
        • reduce progression
        • cardiovascular risk assessment and lifestyle modifications
          • vitamin E 30mg/day supplementation appears to reduce risk of progression 1)
        • avoidance of nephrotoxic medications and volume depletion
    • orange phase CKD:
      • eGFR 45-59 with microalbuminuria, or,
      • eGFR 30-44 with or without microalbuminuria
      • see orange action plan:
        • as for yellow plus:
          • early detection and Mx of complications
          • adjust medication doses for renal impairment
          • referral to nephrologist as needed
    • red phase CKD:
      • macroalbuminuria (urine ACR males >25 or females >35mg/mmol), or,
      • eGFR < 30
      • see red action plan:
        • as for orange plus:
          • prepare for kidney replacement Rx if appropriate
          • prepare for non-dialysis supportive care if appropriate

see also:


  • Cockcroft-Gault formula is no longer recommended when calculating eGFR for the detection of CKD.
  • The CKD-EPI equation is the preferred method for measuring eGFR and has been shown to have greater accuracy and precision compared to other formulae.
  • 2021 CKD-EPI creatinine-cystatin is recommended as a confirmatory test in patients at extremes of body type (e.g. obese patients, high or low muscle mass)
  • elevated urine ACR is a more common sign of CKD than a decreased eGFR. In a 2013 Australian Health Survey, 8% of adults had abnormal urine ACR, while 4% had an abnormal eGFR result

clinical situations where eGFR results may be unreliable and/or misleading for CRF:

  • NB. basis for eGFR estimates is on serum creatinine levels as:
    • creatinine is generated in muscle and is proportionate to muscle mass and production remains relatively constant
    • 85-90% of creatinine is excreted by the kidney; the rest undergoes tubular secretion
  • Unreliable results as indicator for CRF may be due to either:2)
    • Acute changes in kidney function (e.g. AKI).
    • People on dialysis
    • increased or decreased production of creatinine
      • Recent consumption of cooked meat (consider re-assessment when the individual has fasted or specifically avoided a cooked meat meal within 4 hours of blood sampling).
      • Exceptional dietary intake (e.g. vegetarian diet, high protein diet, creatine/creatinine supplements).
      • Extremes of body size.
      • Conditions of skeletal muscle, paraplegia, or amputees (may overestimate eGFR).
      • High muscle mass (may underestimate eGFR).
      • intense exercise can increase creatinine by increasing muscle breakdown
      • rhabdomyolysis - NB. this can also cause serious AKI via a different mechanism
      • Children under the age of 18 years.
    • interference with the Jaffe assay that is used to measure serum creatinine
      • can be influenced by other endogenous chromogens such as acetone and acetoacetate (such as in diabetic ketoacidosis), fasting, lipaemia, and haemolysis, resulting in an overestimate of the serum creatinine
      • drugs that can interfere with the assay include IV cefoxitin and IV cefazolin; barbiturates; N-acetylcyteine;
      • another material known to interfere with the Jaffe reaction is nitromethane, a common component of radio-controlled-vehicle fuels
      • high IgM paraprotein levels due to lymphoplasmacytoid lymphoma 3)
    • decreased tubular secretion of creatinine
      • drugs interacting with creatinine excretion (e.g. fenofibrate although can also cause AKI, trimethoprim, cimetidine, ranitidine, high dose steroids).
    • Severe liver disease present.
    • eGFR values above 90 mL/min/1.73m2
    • Pregnancy
    • Minor changes in eGFR could be due to physiological or laboratory variability
      • serum creatinine can vary by 0.5 to 1.0 mg/dL according to diurnal and menstrual variations, race, fasting status, and diet (and method of meat preparation)

drug-induced renal disease

acute kidney injury (AKI)

  • many drugs implicated
    • the kidneys normally receive 25% of all cardiac output
    • roles of prostaglandins in the kidneys:
      • vasodilatory actions:
        • mainly prostacyclins, PGE2, PGD2 - will act as vasodilators in the afferent arteriole, increasing renal perfusion, with distribution of the cortex flow to the nephrons in the renal medullary region
        • this is a counter regulation of mechanisms, such as the renin-angiotensin-aldosterone system and that of the sympathetic nervous system to ensure adequate renal perfusion
      • PGE2 will also inhibit the transport of sodium and chloride in the ascending loop of Henle and in the collecting ducts, by means of stimulating of the EP1 receptor, leading to natriuresis
      • PGE2 exerts an antagonistic action on the antidiuretic hormone (ADH) receptors, also promoting diuresis
    • NSAID cyclooxygenase (COX) enzyme inhibition prevents the above actions of prostaglandins resulting in reduce renal perfusion, medullary ischaemia, reduced natriuresis, reduced diuresis and thus may potentially cause salt and water retention
    • mechanisms of NSAID AKI:
      • haemodynamically mediated due to inadequate renal perfusion
        • risk factors:
          • volume depletion (eg. diuretics or dehydration) + ACEIs + NSAIDs
          • high dose NSAIDs in the elderly
          • systemic arterial hypertension, which causes an even higher activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, leading to vasoconstriction; and the inhibition of prostaglandin synthesis causes the loss of the compensatory mechanism of renal vasodilation
          • comorbidities that lead to a decrease in effective arterial volume, such as nephrotic syndrome with a high level of proteinuria, liver cirrhosis, especially in those with ascites, heart failure and lupus nephritis.
      • immune related acute interstitial nephritis, which may manifest as nephrotic proteinuria
        • in the future this could potentially be diagnosed by finding the protein CXCL-9 in the urine 4)
    • long-term NSAID use can lead to chronic kidney disease (CKD)
      • this is mainly dose dependent in those with co-morbidities
      • in patients without renal disease, young and without comorbidities, NSAIDs are not greatly harmful however care should be given in chronic use
    • most of the side effects of NSAIDs are related to COX-1 inhibition, individuals with previously compromised renal function are the most affected by the time-dependent use of non-selective NSAIDs rather than Cox-2 inhibitors
    • however, the action of COX-2 is associated with water and electrolytic maintenance in the renal environment, which worsens its effects under dehydration, low renal perfusion or previously existing renal damage.
  • dose-related direct nephrotoxicity:
    • amphotericin B, gentamicin
  • hypersensitivity
    • penicillins, sulphonamides
  • obstructive uropathy due to crystal formation
    • sulphonamides
  • osmotic nephrosis
    • low Mw dextran
  • tetracyclines
    • 2 mechanisms:
      • renal failure
      • Fanconi syndrome

drug-induced LE

nephrotic syndrome

papillary necrosis

  • analgesic abuse

retro-peritoneal fibrosis

  • methysergide, ergotamine, methyldopa

metabolic effects


  • renal pelvis mesothelial tumour eg. analgesics

aetiology of small kidneys

  • chronic glomerulonephritis (GN) - regular outline
  • chronic acute pyelonephritis - irregular outline
  • other chronic nephropathy eg. interstitial nephritis
  • renal artery stenosis
  • atrophy following chronic obstruction
  • congenital renal hypoplasia

aetiology of large kidneys

renal.txt · Last modified: 2024/02/23 22:43 by gary1

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