Severe Acute Renal Failure Research Articles

Severe acute renal failure following high-dose methotrexate therapy in adults with haematological malignancies: a significant number result from unrecognized co-administration of several drugs

Severe acute renal failure following high-dose methotrexate therapy in adults with haematological malignancies: a significant number result from unrecognized co-administration of several drugs

Pyelonephritis Presenting with Severe Acute Renal Failure

We describe an unusual case of an 8-yr-old child presenting with low grade fever and acute renal failure. Investigations showed blood urea 246 mg/dl, serum creatinine 6.4 mg/dl, microscopic hematuria and 2+ proteinuria. Renal biopsy was done in view of rapidly worsening kidney function and showed dense lymphoplasmacytic infiltrate and neutrophils with focal areas of interstitial necrosis, confirming acute pyelonephritis. Ultrasonography and MRI demonstrated multiple renal abscesses. He was managed with antimicrobial therapy and hemodialysis.

Treatment of metformin-associated lactic acidosis with sustained low-efficiency daily dialysis.

Sir, Sustained low-efficiency daily dialysis (SLEDD) is an intermittent prolonged dialysis modality which is increasingly used for the treatment of acute renal failure [1,2], as it combines most of the advantages of both the classic intermittent treatments and the continuous modalities in terms of safety, efficacy, haemodynamic stability and costs. GENIUS® 90 Therapy System (GENIUS) (Fresenius Medical Care, Bad Homburg, Germany) gained interest for application in SLEDD for the treatment of acute renal failure [1,2] as well as of acute drug intoxication [3–6]. No published experience exists about the use of SLEDD in metformin-associated lactic acidosis (MALA). Here we report the case of a 64-year-old diabetic woman who on 12 November 2007 was admitted to the gynaecology unit of our hospital in order to undergo a surgical intervention for the correction of hysterocele, cystocele and enterocele. On 14 November 2007 she underwent colpohysterectomy, McCall culdoplasty, urethrocystopexy and colpoperineoplasty. Her past medical history included mild chronic renal failure (serum creatinine levels were between 1.3 and 1.5 mg/dl), arterial hypertension and type II diabetes mellitus. At the time of admission she was being treated with the following drugs (daily doses): metformin 3000 mg, allopurinol 300 mg, verapamil 120 mg, irbesartan 300 mg and furosemide 25 mg. On 17 November serum creatinine level was 1.4 mg/dl; on 18 November the patient became oliguric, confused and started to be affected by nausea, vomiting, abdominal pain and anorexia. On 19 November serum creatinine level was 5.7 mg/dl and liver enzymes were normal. Irbesartan and metformin therapy were stopped. A renal ultrasound showed normal kidney volume with districtly reduced thickness, a small increase of echogenicity and no hydronephrosis. In the evening, the patient became anuric and presented diffuse oedema, rales at lung bases and tachypnoea. Drowsiness appeared. She was hypoglycaemic at 50 mg/dl; blood pressure was 90/40 mmHg; the serum creatinine level was 7.4 mg/dl. Lactic acidosis was diagnosed: pH 7.16, serum bicarbonate level 11.1 mmol/l, serum lactate level 13.8 mmol/l (normal values: 0.5–1.6 mmol/l). A double lumen 12 F central venous catheter was positioned in the left femoral vein and a 10-h SLEDD session with GENIUS was started. A low-flux polysulfone membrane (F7; surface area 1.6 m2; Fresenius Medical Care, Bad Homburg, Germany) was applied, blood/dialysate flow was set at 120 ml/min and the ultrafiltration rate at 150 ml/h. Anticoagulation of the circuit was obtained with heparin 5000 IU/treatment. Dialysate composition was as follows: calcium, 1.5 mmol/l; magnesium, 0.5 mmol/l; potassium, 3 mmol/l; sodium, 140 mmol/l; bicarbonate, 35 mmol/l; chloride, 111.5 mmol/l; hydrochloric acid, 2.0 mmol/l; glucose, 5.5 mmol/l and citrate, 0.084 mmol/l. At the start of the SLEDD session, blood pressure was 100/50 mmHg and was constant during the treatment. Blood samples were collected every hour for the serum bicarbonate and lactate level measurement. Five hours after the end of the first GENIUS treatment, the patient started a new 8-h SLEDD session with GENIUS (on 20 November), and on 21 November a further 6-h SLEDD session with GENIUS was started 18 h after the end of the second session. Serum bicarbonate and lactate levels are shown in Figure ​Figure1.1. There was a rapid decrease in serum lactate levels and the reciprocal increase in serum bicarbonate levels during the three SLEDD sessions. A complete normalization of acid–base balance and of serum lactate levels with cessation of anuria was observed after three treatments. On 23 November, pH was 7.41, serum bicarbonate levels 24.5 mmol/l and serum lactate levels 1.5 mmol/l. On 29 November the patient was discharged from the hospital with serum creatinine levels of 2.9 mg/dl. After 3 months her serum creatinine levels were back to 1.4 mg/dl. In conclusion, SLEDD with GENIUS is able to offer an adequate and well-tolerated dialysis treatment for the therapy of MALA associated with severe oligoanuric acute renal failure. Fig. 1 Hourly measurements of serum lactate (•) and bicarbonate levels (⧫) during the three sessions of SLEDD with GENIUS. Conflict of interest statement. None declared.

Long-Term Outcomes of Acute Kidney Injury

Acute kidney injury (AKI) is common in the intensive care unit and is associated with significant morbidity and mortality. Based on the RIFLE criteria, AKI occurs in up to 67% of patients in the intensive care unit (ICU), with approximately 4% of critically ill patients requiring renal replacement therapy (RRT). It is well known that this subset of AKI patients who require RRT have an in-hospital mortality rate exceeding 50%. However, long-term outcomes of survivors of AKI requiring RRT remain poorly described. Long-term mortality is greater in those patients who survived AKI when compared with critically ill patients without AKI. Long-term morbidity, renal and extrarenal, is a frequent and underappreciated complication of AKI. Among survivors of AKI at long-term follow-up (1-10 years), approximately 12.5% are dialysis dependent (wide range of 1%-64%, depending on the patient population) and 19% to 31% have chronic kidney disease. According to the United States Renal Data System, "acute tubular necrosis without recovery" as a cause of end-stage kidney disease increased from 1.2% in 1994 to 1998 to 1.7% in 1999 to 2003. The incidence will likely continue to rise with the aging population, increase in comorbidities, and expansion of intensive care unit capabilities. AKI is an underrecognized cause of chronic kidney disease (CKD) and patients who survive should be followed closely for new CKD and/or progression of underlying CKD.

Collapsing glomerulopathy and haemophagocytic syndrome related to malaria: a case report

Authors report a 37-year-old Senegalese woman with no known history of nephropathy who was admitted for fever related to malaria, severe acute renal failure requiring dialysis with nephrotic syndrome. Biological examinations and bone marrow aspiration showed hemophagocytic syndrome. A kidney biopsy found a 'collapsing glomerulopathy' (CG). A protracted course of steroids yielded a complete, unexpected remission of the nephrotic syndrome and renal function was normal at 18 months.

Lymphoma-associated hemophagocytic syndrome: a rare cause of severe prerenal acute renal failure

We report on a 79-year-old woman having hemophagocytosis and capillary hyperpermeability syndrome who presented with anuric prerenal acute renal failure. The patient eventually died of a hypovolemic shock. Post-mortem biopsies evidenced a highly aggressive B cell intravascular lymphoma without amyloidosis. Physicians should be aware of the risk of anuric prerenal acute renal failure in the course of lymphoma-associated hemophagocytic syndrome.

Intravascular Hemolysis and Acute Renal Failure After Mitral and Aortic Valve Repair

Intravascular Hemolysis and Acute Renal Failure After Mitral and Aortic Valve Repair

Obstructive nephropathy and kidney injury associated with ketamine abuse

A 26-year-old man presented to the emergency department in a state of collapse. One month prior to the current admission he was seen by a urologist with frank haematuria associated with colicky abdominal pain, increased urinary frequency and dysuria. Although he was initially treated for a urinary tract infection a CT abdomen demonstrated moderate bilateral hydronephrosis. No cause for the hydronephrosis was seen, in particular no calculi. Common bile duct (CBD) was measured at 8 mm. Cystoscopy revealed a diffusely inflamed bladder with marked reduction in capacity (150 cc) but no obstruction at the ureteric orifices. The bladder biopsy showed inflammatory change but no dysplasia or malignancy. No firm diagnosis was reached and the patient was discharged with outpatient follow-up. For 4 days prior to the current admission the patient had been unwell with increasing flank pain, but had become drowsy and short of breath. On arrival, blood pressure was low at 95/60 mmHg with an associated tachycardia (140 bpm, sinus rhythm) and tachypnoea (60 breaths/min). The Glasgow coma scale was 13/15 with no localizing neurological signs. Initial investigations revealed severe metabolic acidosis (pH 7.2, bicarbonate 6.4 mmol/l, pO2 39.3 kPa, pCO2 2.0 kPa) and acute renal failure (serum potassium 5.4 mmol/l, urea 36.7 mmol/l, creatinine 851 μmol/l). Liver function tests were abnormal with an obstructive pattern (serum bilirubin 58 μmol/l, alkaline phosphatase 294 IU/l, alanine transaminase 106 IU/l, γGT 1045 IU/l). Further history revealed that the patient was a regular user of street ketamine intra-nasally for the past 2 years.

Acid-base Balance in Combined Severe Hepatic and Renal Failure: A Quantitative Analysis

Severe hepatic failure (SHF) commonly leads to major changes in acidbase balance status. However, the direct effects of liver failure per se on acid base balance are poorly understood because this condition is usually associated with acute renal failure (ARF). To assess the effect of SHF on acid-base balance. Retrospective laboratory investigation. Thirty-seven critically ill patients with SHF complicated by ARF, and 42 patients with severe ARF without liver failure prior to renal replacement therapy. Retrieval of clinical and laboratory data from prospective unit and laboratory databases. Quantitative acid-base assessment using Stewart-Figge methodology. Comparison of findings between the two groups. Comparison of demographic and clinical features. Patients with combined SHF and ARF were younger and had significantly higher mean bilirubin, ALT and INR levels (p<0.0001). Their mean lactate concentration was higher (6.4 vs. 2.1 mmol/L; p<0.0001) leading to a greater anion gap (25.8 vs. 16.1 mmol/L; p<0.0001). The ionized calcium concentration (1.00 vs. 1.15 mmol/L; p<0.0001) was lower but the strong ion difference apparent (SIDa) was greater (42.0 vs. 38.0 mEq/L; p<0.005) due to hypochloremia. The albumin concentration was low but higher than in control patients (28 vs. 24 g/L; p<0.01) and the calculated strong ion gap (SIG) was greater (12.6 vs. 9.3 mEq/L; p<0.01). The base excess was similar to controls and the pH was preserved in the near normal range by marked hypocapnea. Combined SHF and ARF is a syndrome with unique acid-base changes due mostly to lactic metabolic acidosis and, in smaller part, to the accumulation of unmeasured anions. This acidosis, like that of ARF, is attenuated by hypoalbuminemia, by a unique preservation of the SIDa due to hypochloremia, and by marked hypocapnea.

An overview of drug-induced acute kidney injury

The complex nature of critical illness often necessitates the use of multiple therapeutic agents, many of which may individually or in combination have the potential to cause renal injury. The use of nephrotoxic drugs has been implicated as a causative factor in up to 25% of all cases of severe acute renal failure in critically ill patients. Acute tubular necrosis is the most common form of renal injury from nephrotoxin exposure, although other types of renal failure may be seen. Given that this is a preventable cause of a potentially devastating complication, a comprehensive strategy should be used to avoid nephrotoxicity in critically ill patients including: accurate estimation of pre-existing renal function using serum creatinine-based glomerular filtration rates, avoidance of nephrotoxins if possible, ongoing monitoring of renal function, and immediate discontinuation of suspected nephrotoxins in the event of renal dysfunction.

Schwere Cholestase mit Nierenversagen durch Anabolika bei einem Bodybuilder

A 28-year-old body builder was admitted because of jaundice. For 80 days, until 3 weeks before hospitalization, he had been taking moderately high doses of anabolic steroids: metandienone (methandienone), 10-50 mg daily by mouth, and stanozolol, 50 mg intramuscularly every other day. Physical examination was unremarkable except for yellow discoloration of the skin and sclerae. Bilirubin concentration was raised to 4.5 mg/dl, cholestasis enzymes were normal, while transaminase activities were raised. Liver biopsy was compatible with cholestasis induced by anabolic steroids. Although the steroids had been discontinued, the patient's general condition deteriorated over 7 weeks. Serum bilirubin rose up to a maximum of 77.9 mg/dl. In addition renal failure developed with a creatinine concentration of 4.2 mg/dl. The patient's state improved simultaneously with the administration of ursodeoxycholic acid and the biochemical values gradually reached normal levels after several weeks. Anabolic steroids can cause severe cholestasis and acute renal failure. In this case there was a notable temporal coincidence between the administration of ursodeoxycholic acid and the marked clinical improvement.

Rituximab for passenger lymphocyte syndrome associated with allogeneic SCT

Immune-mediated hemolytic anemia is one of the possible complications after both solid organ and allogeneic SCT (ASCT), potentially associated with significant morbidity, including severe hemolysis and acute renal failure.1 Death from massive hemolysis has also been reported in the literature.2 Passenger lymphocyte syndrome (PLS) is occasionally a cause of hemolysis in these patients. PLS occurs between day 5 and 15 post transplant when a minor ABO incompatibility exists between the donor and the recipient (most common A+ recipient, O+ donor). Immunocompetent donor B-lymphocytes transferred passively with the graft maintain their ability to generate antibodies, which bind to the recipient's RBCs causing hemolysis.3, 4, 5, 6 The treatment of PLS has been mainly supportive, with or without immunosuppression.1, 6 This report describes the first experience with the use of rituximab (Rituxan, Genentech, South San Francisco, CA, USA) for the treatment of PLS in an ASCT patient and reviews the accumulated data regarding the transfusion requirement for patients with PLS after ASCT.

Glomerulonephritis causing acute renal failure during the course of bacterial infections. Histological varieties, potential pathogenetic pathways and treatment

To illustrate diagnostic approaches, potential pathogenetic differences, epidemiological implications and therapeutic dilemmas posed by glomerulonephritis (GN) with acute renal failure (ARF) complicating bacterial infections, we analyzed the course of four male patients, aged 53-71 years, who developed GN and ARF following bacterial infections. The first two patients developed GN with immunoglobulin A (IgA) deposits after infections with hospital-acquired methicillin resistant Staphylococcus aureus (MRSA). Clinical, serologic and histological features, classification of GN and treatment differed between the two patients. In the first patient, serological features (transient hypocomplementemia, normal serum protein electrophoresis) and histological findings were consistent with typical post-infectious GN. Treatment with antibiotics alone resulted in normalization of the renal function despite the severity of ARF, which required temporary hemodialysis. In the second patient, serological features (normal serum complement, polyclonal elevation of gamma globulins) and histological picture of the kidneys were characteristic of IgA nephropathy with fibrocellular crescents, and skin histology was consistent with vasculitis. Cyclophosphamide and corticosteroids were added to the antibiotics, with partial improvement of the renal failure. The third patient developed simultaneous acute rheumatic fever and post-streptococcal GN causing severe ARF requiring hemodialysis. Complete recovery of ARF and migratory polyarthritis followed initiation of corticosteroids. The fourth patient developed ARF and cerebral vasculitis following a prolonged course of Streptococcus mutans endocarditis with delayed diagnosis. He also developed multiple serological abnormalities including elevated titers of antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies (ANA), anti-phospholipid antibodies, rheumatoid factor, and modest hypocomplementemia. Kidney biopsy revealed ANCA-mediated focal GN with 10% crescents and acute interstitial nephritis. Treatment with cyclophosphamide plus corticosteroids, but not with antibiotics alone, resulted in resolution of both the ARF and the features of cerebral vasculitis. GN following bacterial infections may have various pathogenetic mechanisms, presents complex diagnostic challenges, may be preventable in the case of hospital-acquired MRSA, and, in addition to antibiotics, may require immunosuppressive therapy in carefully selected and monitored cases.

Role of Tissue Kallikrein in Prevention and Recovery of Gentamicin-Induced Renal Injury

Gentamicin is an aminoglycoside antibiotic that induces severe nephrotoxicity and acute renal failure. In the current project, we investigated the protective effects of tissue kallikrein (TK) protein administration (1 mug/h via osmotic minipumps) on kidney damage, apoptosis, and inflammation both during and after a 10-day regimen of gentamicin (80 mg/kg body weight/day sc) in Sprague-Dawley rats. TK infusion during gentamicin treatment significantly attenuated drug-induced renal dysfunction, cortical damage, and apoptosis. Moreover, TK reduced inflammatory cell accumulation in conjunction with diminished superoxide production and decreased expression of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and intercellular adhesion molecule-1. The protective effects of TK were blocked by coinfusion of icatibant (1.3 mug/h), indicating a kinin B2 receptor-mediated signaling event. After cessation of gentamicin treatment, TK infusion for 2 weeks completely restored kidney histology and morphology comparable to that of saline-treated animals. Furthermore, TK reduced gentamicin-induced renal dysfunction and fibrosis as evidenced by decreased myofibroblast and collagen accumulation in the kidney. In vitro, gentamicin increased the number of apoptotic cells and caspase-3 activity, but decreased phosphorylation of the prosurvival kinase Akt, in immortalized rat proximal tubular cells; addition of TK and bradykinin prevented these effects. In conclusion, our findings indicate that kallikrein/kinin prevents and promotes recovery of gentamicin-induced renal injury by inhibiting apoptosis, inflammatory cell recruitment, and fibrotic lesions through suppression of oxidative stress and proinflammatory mediator expression in animals during and after gentamicin treatment.

Histological Features of Acute Tubular Necrosis in Native Kidneys and Long-Term Renal Function

There are few studies on the relationship between the morphology of acute tubular necrosis (ATN) in native kidneys and late functional recovery. Eighteen patients with acute renal failure (ARF) who had undergone renal biopsy were studied. All had the histological diagnosis of ATN and were followed for at least six months. Clinical characteristics of ARF were analyzed, and histological features were semi-quantitatively evaluated (tubular atrophy, interstitial inflammatory infiltrate, interstitial fibrosis, and ATN). According to the maximal GFR achieved during the follow-up, patients were divided into two groups: complete recovery (GFR ≥ 90 mL/min/1.73 m2) and partial recovery (GFR < 90 mL/min/1.73 m2). Only 39% of the patients achieved complete recovery. Patients with partial recovery achieved their maximal GFR (63 ± 9 mL/min/1.73 m2) 37 ± 14 months after ARF, a period of time similar to those patients with complete recovery (i.e., 54 ± 22 months). Patients with partial recovery had more severe ARF: oliguria was more frequent (90 versus 17%, p < 0.01), and they had higher peak creatinine (13.85 ± 1.12 versus 8.95 ± 1.30 mg/dL, p = 0.01), and longer hospitalization (45 ± 7 versus 20 ± 4 days, p = 0.03). No single histological parameter was associated with partial recovery, but the sum of all was when expressed as an injury index [4.00 (2.73–5.45) versus 2.00 (1.25–3.31), p < 0.05]. In conclusion, among patients with atypical ATN course, those with more severe ARF and tubule-interstitial lesions are more prone to partial recovery.

Fenofibrate-Induced Acute Renal Failure Due to Massive Rhabdomyolysis after Coadministration of Statin in Two Patients

Fibric acid derivatives and statins have been increasingly recognized as causes of rhabdomyolysis and acute renal failure. We report severe rhabdomyolysis and acute renal failure associated to combination treatment with statin and fenofibrate in two patients with underlying coronary artery disease. Both patients developed rhabdomyolysis-induced acute renal failure after their hyperlipidemia treatment was changed from statin to statin plus fenofibrate. Both patients experienced intense muscle symptoms, hemoglobinuria, oliguria, and elevation of blood urea nitrogen and serum creatinine. Their serum creatine kinase levels were markedly elevated (case 1; 97,392 IU/l and case 2; 96,639 IU/l). Rhabdomyolysis induced acute renal failure was diagnosed in both patients. Both patients were managed with cessation of the statin-fibrate combination, adequate fluid resuscitation and forced alkaline-mannitol diuresis. Although both patients required hemodialysis, their renal function recovered. Fenofibrate initiation is associated with an increased risk for rhabdomyolysis in patients receiving statin therapy. To prevent future events, it is crucial that clinicians recognize the interaction risk associated with concurrent use of statin and fenofibrate. We recommend careful monitoring when fenofibrate is given to patients receiving statin therapy.

Severe rhabdomyolysis and acute renal failure secondary to the use of simvastatin in undiagnosed hypothyroidism

A 52-year-old Indian woman with underlying diabetes mellitus, hyperlipidemia and undiagnosed hypothyroidism presented with generalized musculoskeletal pain and oliguria for three days. The patient was taking 80 mg of simvastatin (initiated 20 days before) after cardiac catheterization for an inferior myocardial infarction. Laboratory evaluation revealed the following serum levels: creatine kinase, 81,660 U/L; aspartate aminotransferase, 2,497 U/L; alanine aminotransferase, 1,304 U/L; blood urea nitrogen, 88 mg/dL; creatinine, 5.1 mg/dL; free thyroxine (FT4), 12.6 Pmol/L and thyroid stimulating hormone, 22.7 uIU/L. Simvastatin was discontinued and the patient was administered forced alkaline diuresis. Her hypothyroidism was treated with thyroxine, which was continued after discharge. Her renal function recovered within two months. This case report discusses the higher incidence of rhabdomyolysis in patients with undiagnosed hypothyroidism receiving large doses of simvastatin.

On the Mechanisms Underlying Poisoning-Induced Rhabdomyolysis and Acute Renal Failure

ABSTRACTThe clinical syndrome of rhabdomyolysis is caused by injury of skeletal muscles resulting in release of intracellular muscle constituents. Drug poisoning is one of the causes of severe rhabdomyolysis. Severe electrolyte disorders and acute renal failure may occur in rhabdomyolysis, leading to life-threatening situations. Early initiation of renal replacement therapy can help improve outcome.In the present retrospective study, medical records of 181 patients suspected of rhabdomyolysis from Loghman-Hakim Hospital in the period of 2004 to 2005 were reviewed. A creatinine phosphokinase (CPK) value of greater than five times normal (≥975 IU/L) was the basis for confirmation of a rhabdomyolysis diagnosis. An increased serum creatinine level of more than 30% was the basis for acute renal failure diagnosis.Out of 156 patients, 100 were male with an age range of 13 to 78 years. One hundred and two (92%) patients had CPK >975 U/L, and 36 patients (28.6%) had a 30% or more increase in their creatinine level during their admission days. Mean fluid intake was the same in patients with renal failure and those without renal failure. In 8.3% of the cases, multiple drug poisoning was observed. The most common compound overdose associated with rhabdomyolysis was opium.It is concluded that fluid therapy alone is not adequate in the management of acute renal failure in rhabdomyolysis. Therefore, other etiological factors are involved that remain to be elucidated by further studies.

Renal Thrombotic Microangiopathies Induced by Severe Hypertension

Renal thrombotic microangiopathy (TMA) is an uncommon vascular complication of severe hypertension. Until now, its clinical-pathological characteristics and renal survival have been unclear. Twenty-one patients with biopsy-proven renal TMA and with severe or malignant hypertension were retrospectively studied. All the patients exhibited severe hypertension, with systolic blood pressure at 200-280 mmHg and diastolic pressure at 110-180 mmHg. No patients had hemorrhagic manifestations. Elevated lactate dehydrogenase and thrombocytopenia were found in 6 and 5 patients, respectively. Significant proteinuria (>3 g/day) was present in 2 patients and microscopic hematuria in 18 patients. All patients presented with renal insufficiency (creatinine 3.1+/-2.1 mg/dL). The level of von Willebrand factor:antigen (vWF:Ag) in patients was not significantly higher than that in the healthy subjects, while the ADAMTS13 (a disintegrin and metalloprotease, with thrombospondin-1-like domains) activity was not significantly lower than that in the healthy subjects. Renal histology showed a TMA involving preglomerular arterioles and/or interlobular arteries characterized by fibrin deposits and vascular wall sclerosis. Fibrin glomerular microthrombi were not observed in these patients. Four patients required hemodialysis upon admission for severe acute renal failure. On follow-up, 3 patients had recovered normal renal function and 14 had mild renal insufficiency (creatinine 1.8+/-0.3 mg/dL), while 4 patients still required persistent hemodialysis. In conclusion, compared with patients having hemolytic uremic syndrome/thrombocytopenic purpura, our patients showed a low incidence of thrombocytopenia and better renal outcome.

Acute Renal Failure in Intensive Care Burn Patients (ARF in Burn Patients)

The purpose of this study was to establish the incidence and mortality of burn patients with acute renal failure (ARF) at the Helsinki Burn Centre and to analyze the associated factors. The files of 238 intensive care (ICU) patients of a total of 1380 burn patients admitted to our institution between November 1988 and December 2001 were studied retrospectively. Of all admitted burn patients, 17.2% needed ICU. According to our criteria (S-Cr >120 micromol/l = 1.4 mg/dl), 39.1% of the ICU patients suffered from ARF and one in three of these required renal replacement therapy. The proportion of all admitted burn patients requiring renal replacement therapy was 2.3%. The mortality of ICU patients with ARF was 44.1% whereas that of patients without ARF was only 6.9%. Renal function recovered in all survivors. The nonsurvivors had a larger burned total body surface area, were older, and had more inhalation injuries and a higher abbreviated burn severity index score. The prognosis for patients with early ARF was worse than that for patients with late ARF. Rhabdomyolysis caused by flame injury was associated with high mortality. In this study we observed that ARF is associated with higher mortality even in minor burns when compared with patients without ARF. Flame burn with rhabdomyolysis and subsequent ARF predicts very poor survival. If a patient with severe ARF survives, the renal failure recovers over time.