Acute renal failure
Acute renal failure (ARF), also known as acute kidney failure or acute kidney injury, is a rapid loss of
renal functiondue to damage to the kidneys, resulting in retention of nitrogenous ( ureaand creatinine) and non-nitrogenous waste products that are normally excreted by the kidney. Depending on the severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic disturbances, such as metabolic acidosis(acidification of the blood) and hyperkalaemia(elevated potassium levels), changes in body fluid balance, and effects on many other organ systems. It can be characterised by oliguriaor anuria(decrease or cessation of urine production), although "nonoliguric ARF" may occur. It is a serious disease and treated as a medical emergency.
Acute renal failure is usually categorised (as in the
flowchartbelow) according to "pre-renal, renal" and "post-renal" causes.
* "Pre-renal" (causes in the blood supply):
hypovolemia(decreased blood volume), usually from shock or dehydrationand fluid loss or excessive diuretics use.
hepatorenal syndromein which renal perfusionis compromised in liver failure
** vascular problems, such as atheroembolic disease and
renal vein thrombosis(which can occur as a complication of the nephrotic syndrome)
infectionusually sepsis, systemic inflammation due to infection
* "Renal" (damage to the kidney itself):
toxins or medication(e.g. some NSAIDs, aminoglycosideantibiotics, iodinated contrast, lithium, phosphate nephropathydue to bowel preparation for colonoscopywith sodium phosphates)
rhabdomyolysis(breakdown of muscle tissue) - the resultant release of myoglobinin the blood affects the kidney; it can be caused by injury(especially crush injury and extensive blunt trauma), statins, stimulants and some other drugs
hemolysis(breakdown of red blood cells) - the hemoglobindamages the tubules; it may be caused by various conditions such as sickle-cell disease, and lupus erythematosus
multiple myeloma, either due to hypercalcemiaor "cast nephropathy" (multiple myeloma can also cause chronic renal failureby a different mechanism)
glomerulonephritiswhich may be due to a variety of causes, such as anti glomerular basement membrane disease/ Goodpasture's syndrome, Wegener's granulomatosisor acute lupus nephritis with systemic lupus erythematosus
* "Post-renal" (obstructive causes in the urinary tract) due to:
medicationinterfering with normal bladder emptying.
benign prostatic hypertrophyor prostate cancer.
** due to abdominal malignancy (e.g.
ovarian cancer, colorectal cancer).
In general, renal failure is diagnosed when either
creatinineor blood urea nitrogentests are markedly elevated in an ill patient, especially when oliguria is present. Previous measurements of renal function may offer comparison, which is especially important if a patient is known to have chronic renal failureas well. If the cause is not apparent, a large amount of blood tests and examination of a urinespecimen is typically performed to elucidate the cause of acute renal failure, medical ultrasonographyof the renal tract is essential to rule out obstruction of the urinary tract.
Consensus criteria [cite journal |author=Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P |title=Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group |journal=Crit Care |volume=8 |issue=4 |pages=R204–12 |year=2004 |pmid=15312219 |pmc=522841 |doi=10.1186/cc2872 |url=] [cite journal |author=Lameire N, Van Biesen W, Vanholder R |title=Acute renal failure |journal=Lancet |volume=365 |issue=9457 |pages=417–30 |year=2005 |pmid=15680458 |doi=10.1016/S0140-6736(05)17831-3 |url=] for the diagnosis of ARF are:
* Risk: serum creatinine increased 1.5 times OR urine production of <0.5 ml/kg body weight for 6 hours
* Injury: creatinine 2.0 times OR urine production <0.5 ml/kg for 12 h
* Failure: creatinine 3.0 times OR creatinine >355 μmol/l (with a rise of >44) or urine output below 0.3 ml/kg for 24 h
* Loss: persistent ARF or more than four weeks complete loss of kidney function
biopsymay be performed in the setting of acute renal failure, to provide a definitive diagnosis and sometimes an idea of the prognosis, unless the cause is clear and appropriate screening investigations are reassuringly negative.
Acute renal failure may be reversible if treated promptly and appropriately. Resuscitation to normotension and a normal
cardiac outputis key. The main interventions are monitoring fluid intake and output as closely as possible; insertion of a urinary catheter is useful for monitoring urine output as well as relieving possible bladder outlet obstruction, such as with an enlarged prostate. In the absence of fluid overload, administering intravenous fluids is typically the first step to improve renal function. Fluid administration may be monitored with the use of a central venous catheterto avoid over- or under-replacement of fluid. If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomyor urinary catheter) may be necessary. Metabolic acidosisand hyperkalemia, the two most serious biochemical manifestations of acute renal failure, may require medical treatment with sodium bicarbonateadministration and antihyperkalemic measures, unless dialysisis required.
Should hypotension prove a persistent problem in the fluid replete patient,
inotropes such as norepinephrineand/or dobutaminemay be given to improve cardiac outputand hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamineis of any specific benefit, [cite journal |author=Holmes CL, Walley KR |title=Bad medicine: low-dose dopamine in the ICU |journal=Chest |volume=123 |issue=4 |pages=1266–75 |year=2003 |pmid=12684320|doi=10.1378/chest.123.4.1266] and at least a suggestion of possible harm. A Swan-Ganz cathetermay be used, to measure "pulmonary artery occlusion pressure" to provide a guide to left atrial pressure (and thus left heart function) as a target for inotropic support.
The use of
diureticssuch as furosemide, while widespread and sometimes convenient in ameliorating fluid overload, does not reduce the risk of complications and death. [cite journal |author=Uchino S, Doig GS, Bellomo R, "et al" |title=Diuretics and mortality in acute renal failure |journal=Crit. Care Med. |volume=32 |issue=8 |pages=1669–77 |year=2004 |pmid=15286542|doi=10.1097/01.CCM.0000132892.51063.2F] In practice, diuretics may simply mask things, making it more difficult to judge the adequacy of resuscitation.
Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of
dialysisor hemofiltration. Depending on the cause, a proportion of patients will never regain full renal function, thus having end stage renal failurerequiring lifelong dialysisor a kidney transplant.
Before the advancement of
modern medicine, acute renal failure might be referred to as uremic poisoning. Uremiawas the term used to describe the contamination of the bloodwith urine. Starting around 1847 this term was used to describe reduced urine output, now known as oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra.
Acute renal failure due to
acute tubular necrosis(ATN) was recognised in the 1940s in the United Kingdom, where crush victims during the Battle of Britaindeveloped patchy necrosis of renal tubules, leading to a sudden decrease in renal function. [cite journal |author=Bywaters EG, Beall D |title=Crush injuries with impairment of renal function. |journal=Br Med J |volume= |issue=1 |pages=427-32 |year=1941 |pmid=9527411 |doi= |url=http://jasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=9527411] During the Korean and Vietnam wars, the incidence of ARF decreased due to better acute management and intravenous infusion of fluids. [cite journal |author=Schrier RW, Wang W, Poole B, Mitra A |title=Acute renal failure: definitions, diagnosis, pathogenesis, and therapy |journal=J. Clin. Invest. |volume=114 |issue=1 |pages=5–14 |year=2004 |pmid=15232604 |pmc=437979 |doi=10.1172/JCI22353 |url=]
Chronic kidney disease
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