Lesch-Nyhan syndrome presenting with acute renal failure in a 3-day-old newborn

Acute renal failure developed during the first 3 days after birth in a newborn subsequently diagnosed with hypoxanthine-guanine-phosphoribosyl-transferase (HPRT) deficiency. Fluid infusion and allopurinol therapy normalised renal function and serum uric acid levels. Only a few cases of acute renal failure due to acute hyperuricemic nephropathy related to HPRT deficiency have previously been reported in infants, and there are no reported cases in newborns as young as 3 days old.     

An enormous abdominal mass associated with acute renal failure.

We report a 67-year-old man with acute uric acid nephropathy, secondary to spontaneous tumor lysis syndrome, that presented itself as a huge intra-abdominal tumor that led to acute renal failure, hyperuricemia, and azotemia. Initial finding of hydronephrosis detected by ultrasonography led us to believe that the azotemia and decreasing amount of urine resulted from obstructive uropathy, a common complication of malignancy, caused by either a direct renal invasion or a urinary outflow tract compression because of a tumor mass effect. However, clinical observations and the response to therapeutic intervention confirmed the diagnosis of spontaneous tumor lysis syndrome, which is a rare cause of acute uric acid nephropathy.     

AN ENORMOUS ABDOMINAL MASS ASSOCIATED WITH ACUTE RENAL FAILURE

We report a 67-year-old man with acute uric acid nephropathy, secondary to spontaneous tumor lysis syndrome, that presented itself as a huge intra-abdominal tumor that led to acute renal failure, hyperuricemia, and azotemia. Initial finding of hydronephrosis detected by ultrasonography led us to believe that the azotemia and decreasing amount of urine resulted from obstructive uropathy, a common complication of malignancy, caused by either a direct renal invasion or a urinary outflow tract compression because of a tumor mass effect. However, clinical observations and the response to therapeutic intervention confirmed the diagnosis of spontaneous tumor lysis syndrome, which is a rare cause of acute uric acid nephropathy.     

Clinical studies on hyperuricemia and gout after transplantation

We performed renal transplantation on 67 patients (living 37, cadaver 30) between November 1975 and December 1987. Twenty-seven of the 67 patients had hyperuricemia (serum uric acid: male greater than or equal to 8.0 mg/dl, female greater than or equal to 7.0 mg/dl) and 2 of them had episodes of gout. However, there was no correlation between serum creatinine and uric acid in 27 hyperuricemic patients. Twelve of 27 hyperuricemic patients were treated with either allopurinol or benzbromarone. These therapies were effective for 9 of them and serum uric acid level controlled well. One of 2 gouty patients developed gout 4 years after cadaveric renal transplantation. She was treated with anodyne and benzbromarone for gout. These treatments were effective and she has been in good condition. We consider it necessary to treat hyperuricemia after renal transplantation and to control serum uric acid well.     

Hyperuricemia after renal transplantation

Hyperuricemia is common in cyclosporine-treated renal allograft recipients. An increased incidence of gout in patients receiving both diuretics and cyclosporine has been reported, but the effect of hyperuricemia on renal allograft function has not been studied. In a prospective, randomized trial of cyclosporine and prednisone versus azathioprine, prednisone, and antilymphocyte globulin for immunosuppression in renal allograft recipients, 105 of 131 cyclosporine and prednisone-treated patients (80 percent) experienced hyperuricemia (serum uric acid level above 8 mg/dl) and 13 of 131 (10 percent) were severely hyperuricemic (serum uric acid level above 14 mg/dl). In contrast, hyperuricemia developed in 63 of 115 patients (55 percent) treated with azathioprine, prednisone, and antilymphocyte globulin (p less than 0.002). Despite the frequent occurrence of hyperuricemia, gout was rare. Clinical gout developed in six patients in the cyclosporine and prednisone group and in 0 patients in the azathioprine, prednisone, and antilymphocyte globulin group between 1 and 43 months (median 22.5 months) after transplantation. Neither severe hyperuricemia nor diuretic therapy were associated with a significantly increased incidence of gout. The mean serum creatinine concentration of severely hyperuricemic patients (all on cyclosporine and prednisone) was similar to that of normouricemic cyclosporine and prednisone patients (1.8 mg/dl versus 1.6 mg/dl, p greater than 0.2), and the severely hyperuricemic patients had a 4-year graft survival rate of 90 percent. Asymptomatic hyperuricemia after renal transplantation does not adversely affect allograft function, requires no specific therapy, and is not a contraindication to use of diuretics.     

Hyperuricemia, gout, and renal function after liver transplantation.

BACKGROUND: Hyperuricemia is a recognized complication of renal and cardiac transplantation, but the development of hyperuricemia and gout following liver transplantation have received less attention. We have retrospectively assessed the prevalence of hyperuricemia in 134 consecutive liver transplant recipients. RESULTS: Forty-seven percent of the liver transplant recipients studied had hyperuricemia. Serum creatinine was higher in hyperuricemic than in nonhyperuricemic patients. Peak uric acid correlated significantly with corresponding serum creatinine (rs=0.694). Only 6% developed gout. All the patients with gout and 10 hyperuricemic patients with renal impairment but without gout were treated with allopurinol. Over a median period of 3 months, mean serum creatinine fell from 177 micromol/l to 160 micromol/l (P=0.01), without change in type or dose of immuno-suppression. CONCLUSIONS: There is an important association between liver transplantation and hyperuricemia. Treatment with allopurinol results in a significant reduction in serum creatinine in patients with gout and in those with hyperuricemia and renal impairment.     

Potassium citrate administration ameliorates tubulointerstitial lesions in rats with uric acid nephropathy

Although controversial, chronic uric acid nephropathy is a tubulointerstitial disease capable of developing renal function loss. On the other hand, potassium citrate (KCi) administration has demonstrated to be effective in calcium as well as uric acid nephrolithiasis therapy. Therefore, the aim of the present study was to evaluate the possible benefit of KCi treatment in the prevention or amelioration of renal interstitial damage in uric acid nephropathy. Two-month-old male Sprague-Dawley rats were divided into 3 groups: G1 hyperuricemic (HU), G2 hyperuricemic + KCi (HU+KCi), and G3 KCi. G1 and G2 were fed on oxonic acid (inhibitor of rat liver uricase), and a uric acid supplement, during 4 weeks. G2 and G3 were given 2% KCi in drinking water, and G1 regular tap water and standard rat chow. At the end of the study, renal tissue was processed for light and electron microscopy and immunostaining by alpha-smooth muscle actin (SMA). Tubulointerstitial lesions and the amount of alpha-SMA immunostaining in renal tissue were evaluated by histomorphometric quantitation. Rats belonging to the hyperuricemic groups treated with KCi (G2) showed fewer tubulointerstitial lesions as follows: % tubular atrophy: 1.7 +/- 0.3 versus 7.2 +/- 1.2, p < 0.05; inflammatory cells infiltrate (number of cells/area): 0.6 +/- 0.1 versus 2.4 +/- 0.2, p < 0.01; % interstitial fibrosis (cortex): 3.3 +/- 0.3 versus 9.3 +/- 0.5, p < 0.05; % interstitial fibrosis (medulla): 5.2 +/- 0.3 versus 21.9 +/- 1.2, p < 0.01, lower albuminuria (32.8 +/- 11.2 mg/day versus 128.5 +/- 10.4, p < 0.01), higher creatinine clearance ( 1.36 +/- 0.02 ml/min versus 0.74 +/- 0.01, p < 0.01 ) and less percentage of alpha-SMA in renal tissue (1.8 +/- 0.1 versus 10.5 +/- 1.4, p < 0.05), when compared with the hyperuricemic group not treated with KCi (G1). These data suggest that KCi administration could provide a substantial benefit in the regard to tubulointerstitial lesion and progressive renal damage.     

Exercise-induced acute renal failure with renal hypouricemia: a case report and a review of the literature

A previously healthy 16-year-old boy developed acute renal failure following a track race at a local athletic meeting. Several hours after the run, he expressed pain in the loins with nausea and vomiting. After 3 sessions of hemodialysis, he was referred to our hospital. On admission, serum creatinine was elevated to 2.3 mg/dl without an increase in serum uric acid level. After recovery from acute renal failure (ARF), hypouricemia (0.7 mg/dl) became evident in the patient. One year later, he suffered from ARF after a track race with the highest creatinine levels of 1.1 mg/dl. In order to clarify the cause and prognosis of ARF with renal hypouricemia, we summarized the clinical features in 18 patients previously described and our patient. Serum uric acid levels after recovery from ARF were below 1.0 mg/dl in all patients. Renal biopsy in 9 patients showed acute tubular necrosis in 8 patients and uric acid nephropathy in 1. The short-term prognosis of these patients seemed good, although 5 patients needed to undergo hemodialysis in their ARF courses. However, the recurrence of ARF episodes occurred in 6 patients (31.6%) including our patient, indicating that prevention of ARF might be necessary in these patients. More information is required to establish guidance for prevention of ARF.     

Serum uric acid and renal prognosis in patients with IgA nephropathy

BACKGROUND/AIMS: This study was designed to elucidate the clinical significance of serum uric acid (SUA) and the relationship between hyperuricemia and renal prognosis in IgA nephropathy. METHODS: The correlation between SUA and other clinical parameters were examined in 748 IgA nephropathy patients (432 males and 316 females). Among these patients, 226 (144 males and 82 females) who were followed for more than 5 years were examined for the relationship between hyperuricemia and renal prognosis. RESULTS: In IgA nephropathy, SUA correlated negatively with creatinine clearance (Ccr), and positively with urinary protein and tubulointerstitial damage. SUA was higher in patients with hypertension or diffuse proliferative glomerulonephritis. Hyperuricemia was a risk factor for renal prognosis, both in terms of serum creatinine (p = 0.0025) and Ccr (p = 0.0057). In 56 patients with normal Ccr at renal biopsy, the change of Ccr after more than 8 years was -22.3 +/- 20.8% in 13 patients with hyperuricemia, compared with +2.6 +/- 39.4% in 43 patients without hyperuricemia (p = 0.0238). Hyperuricemia was related independently to deterioration of Ccr (p = 0.0461). CONCLUSION: Hyperuricemia in IgA nephropathy is derived from both glomerular and tubulointerstitial damage, and correlated with hypertension. Hyperuricemia is a risk factor for renal prognosis in IgA nephropathy.     

Hyperuricemia influences chronic cyclosporine nephropathy

BACKGROUND: The observation that long-standing hyperuricemia is associated with chronic tubulointerstitial disease, afferent arteriolopathy, intrarenal vasoconstriction, and increased vascular resistance raises the hypothesis that hyperuricemia might contribute to chronic cyclosporine (CsA) nephropathy. The aim of the present study was to investigate the effect of hyperuricemia on chronic CsA nephropathy. METHODS: Patients who were treated with CsA-based immunsuppressive regimens and underwent a renal biopsy were enrolled in this case-control study. We retrospectively obtained posttransplant baseline serum creatinine, uric acid (UA), mean serum UA, and creatinine values 3 months prior to biopsy. CsA trough levels, mean blood pressure, diuretic and antihypertensive treatment were recorded. Biopsy specimens showing CsA nephropathy (n = 34) were revaluated by a pathologist to score CsA nephropathy according to recent quantitative criteria for calcineurin inhibitor arteriolopathy as proposed by M.J. Mihatsch. RESULTS: As compared with the non-CsA nephropathy group, recipient and donor ages, donor origin and cold ischemia times were similar for the CsA nephropathy group (P > .05). Mean CsA doses, CsA trough (C(0)), and C(2) levels were not different between the groups (P > .05). Systolic and diastolic blood pressure, glomerular filtration rate, diuretic usage, and antihypertensive treatment were also similar in CsA nephropathy and non-CsA nephropathy groups (P > .05). Mean serum UA level within 3 months prior to biopsy in the CsA nephropathy and non-CsA nephropathy groups were 7.5 +/- 1.4 mg/dL versus 5.7 +/- 1.4 mg/dL, respectively (P < .001). CONCLUSION: Hyperuricemia seems to exacerbate CsA-induced nephropathy.     

Suprofen-induced uricosuria. A potential mechanism for acute nephropathy and flank pain

Suprofen, a nonsteroidal anti-inflammatory drug, has been associated with the onset of acute flank pain, hematuria, and transient renal dysfunction after the ingestion of one or two doses, particularly in young males. Potential mechanisms of this nephropathy were evaluated in normal males following ingestion of suprofen (200 mg) on two occasions: the first with ad libitum fluid intake and the second during forced water diuresis. On the first study occasion, creatinine clearance, the fractional excretions of uric acid (FEUA) and sodium (FENa), the urinary concentration of undissociated uric acid, and the urinary excretions of prostaglandins and glomerular and tubular proteins were assessed. On the second occasion, inulin and PAH clearances and FEUA and FENa were determined. Within 90 min after suprofen administration, the FEUA increased from 8.8 +/- 2.6 to 35.5 +/- 9.6% (p less than 0.05). Urine became supersaturated for uric acid during ad libitum fluid intake. Glomerular filtration rate, renal plasma flow, and FENa decreased significantly, while prostaglandin and protein excretions did not change. The findings are consistent with acute uric acid nephropathy as a mechanism of suprofen-induced renal dysfunction.     

Influence of cyclosporine and tacrolimus on serum uric acid levels in stable kidney transplant recipients

Although hyperuricemia is a well-known adverse effect of cyclosporine (CsA) treatment, there are contradictory data regarding the effect of tacrolimus on uric acid levels. The aim of this study was to examine the influences of CsA and tacrolimus-based treatment regimens on serum uric acid levels in 155 renal transplant recipients with normal allograft function who underwent renal transplantation between 1999 and 2002. Serum uric acid levels were recorded at 1, 6, 12, 18, and 24 months follow-up. The patients were treated with CsA-based (n = 73), tacrolimus-based (n = 47), or conversion from CsA-based to tacrolimus-based (n = 35) immunosuppressive regimens. Serum uric acid levels for patients in the CsA and tacrolimus groups were 6.3 +/- 1.6 versus 7.9 +/- 1.9 mg/dL and 6.5 +/- 1.8 versus 8.0 +/- 1.8 mg/dL at the study outset and 24 months, respectively. Both of the treatment regimens showed progressively increasing serum uric acid levels (P < .001). Serum uric acid levels of patients with treatment conversion from CsA to tacrolimus were 8.6 +/- 2.8 mg/dL before conversion and 8.1 +/- 1.9 mg/dL after conversion. There was no alteration in serum uric acid levels after the change of treatment (P > .05). These findings indicate that, compared with CsA, tacrolimus offers no advantage for serum uric acid levels in renal transplant recipients.     

Acute renal failure due to bilateral uric acid lithiasis in infants

Acute renal failure (ARF) is one of the complications of urolithiasis, but the role of medical treatment to relieve urinary obstruction in children with ARF is uncertain. We report on infants with acute obstructive uric acid lithiasis. We describe presentation features as well as diagnosis methods and medical treatment in five infants who were admitted to our institution with ARF due to uric acid lithiasis. The medical treatments for all patients were fluid liberalization, urine alkalinization, and oral allopurinol. Two children underwent urinary diversion. Within 8 h, urine output improved in all patients, and the stones passed spontaneously. All obstructed kidneys were relieved with medical treatment, and no renal sequel remained. So this series has showed a role of medical therapy in acute obstructive uric acid lithiasis.     

IgA肾病患者合并高尿酸血症临床及病理特征分析

目的探讨IgA肾病高尿酸血症的临床病理特征及相关危险因素。 方法选取2010年1月至2015年7月于山西医科大学第二医院行经皮肾穿刺活检确诊为IgA肾病的188例患者,根据血尿酸水平将患者分为正常血尿酸组与高尿酸血症组,收集患者一般资料、尿蛋白定量、肾功能等临床生化指标以及病理指标,并对肾脏病理组织进行牛津病理分型。分析两组患者临床表现、肾脏病理特点,应用多元回归统计学方法分析高尿酸血症发生的影响因素。其他数据采用SPSS13.0软件进行统计分析。 结果本研究中心188例IgA肾病患者中合并高尿酸血症的患者有42例,高尿酸血症发生率为22.3%;高尿酸血症组中男性患者36例,女性患者6例;与正常血尿酸组(男性患者61例、女性患者85例)相比,高尿酸血症组男性患者明显增多(χ²＝25.2,P<0.001)。本组研究IgA肾病患者肾脏组织牛津病理分型以M1E1S0T0多见;与正常血尿酸组比较,高尿酸血症组患者肾小管－间质损伤重,差异有统计学意义(χ²＝5.056,P＝0.025)。肾组织免疫复合物IgA沉积于毛细血管袢者高尿酸血症发生率明显升高(χ²＝44.69,P<0.001)。IgA肾病患者合并高尿酸血症的相关因素为性别、体质量指数、甘油三酯、IgA沉积于毛细血管袢。 结论IgA肾病高尿酸血症的危险因素为男性、肥胖、高甘油三酯血症,并可能与IgA在毛细血管区沉积相关。     

Acute hyperuricemic nephropathy and renal failure after transplantation

This report describes a patient who was treated for rejection of a cadaveric renal allograft with a variety of drugs, including the continuous administration of ciclosporin over a period of 16 months. The patient developed hyperuricemia, attacks of gout and finally a rapidly progressing renal failure 17 months after transplantation. The removed transplanted kidney showed extensive tubular dilatation, intratubular deposits of uric acid crystals and characteristic granulomas. There was also morphologic evidence of transplant glomerulopathy, as well as scattered linear parenchymal (cortical?) scars of the type seen in mild chronic ciclosporin toxicity. Both of these changes undoubtedly contributed to the reduction of renal reserve. However, we propose that prolonged continuous use of ciclosporin was the main factor in the development of hyperuricemia and obstructive hyperuricemic nephropathy and renal failure in this patient. To our knowledge cases of this nature have not been previously reported.     

Exercise-induced acute renal failure associated with renal hypouricaemia: results of a questionnaire-based survey in Japan.

BACKGROUND: A retrospective investigation was conducted to define the clinical features of exercise-induced acute renal failure (ARF) associated with renal hypouricaemia with the aim of clarifying further the clinical features of the disease entity. METHODS: A questionnaire was mailed to 43 institutions in Japan that had experienced case(s) of exercise-induced ARF associated with renal hypouricaemia. Fifty-four patients (48 males and six females) were identified from 38 institutions. RESULTS: Median age at the first episode of ARF was 17 years (range 11-46). The maximal serum uric acid and creatinine levels were 4.40+/-2.49 (range 0.4-13.3) and 5.45+/-3.33 mg/dl (range 1.10-17.7), respectively. The serum uric acid level after recovery was 0.70+/-0.25 mg/dl (range 0.1-1.4). The short-term prognosis seemed to be good and histological findings in 28 patients showed minimal change or acute tubular necrosis except for one patient with chronic lesions. ARF episodes occurred predominantly in September, October and May, mostly after strenuous exercise such as a short-distance race. The first symptoms were nausea/vomiting in 51 episodes, loin pain in 35, abdominal pain in 22, general fatigue in 16 and low-grade fever in seven. Thirteen patients (24.1%) experienced recurrent ARF at various intervals. Univariate and multivariate analyses failed to demonstrate any risk factor of ARF recurrence, although no female patients experienced ARF recurrence. CONCLUSIONS: The reason for the heterogeneity in ARF associated with renal hypouricaemia remains unknown. Further studies, especially on molecular mechanisms, are required to establish the best guidance against ARF recurrence.     

A case of acute renal failure after exercise with renal hypouricemia demonstrated compound heterozygous mutations of uric acid transporter 1

Familial renal hypouricemia is a hereditary disease characterized by extraordinary high renal uric acid (UA) clearance and is associated with acute renal failure (ARF). A 17-year-old Japanese male developed ARF after anerobic exercise. Renal function improved completely after approximately 2 weeks of hydration treatment. After remission, hypouricemia became evident (1.0 mg/dL) from the initial level of UA (4.8 mg/dL) and fractional excretion of uric acid (FEUA) was >50%. His parents showed normal levels of UA and FEUA. Polymerase chain reaction of a urate anion exchanger known to regulate UA level [SLC22A12 gene: UA transporter 1 (URAT1)] demonstrated compound heterozygous mutations (Q297X and R90H). Thus, we describe a Japanese male with hypouricemia complicated by anerobic exercise-induced ARF, with definite demonstration of a genetic abnormality in the responsible gene, URAT1.     

Acute Renal Failure of Obstetrical Origin During 1994 at One Center

Although preventable, acute renal failure (ARF) of obstetrical origin continues to be common in developing countries. During the year 1994, we treated a total of 238 cases of ARF. Of these cases, 43 (18%) were of obstetrical origin. All of the patients were known to be previously healthy. Acute renal failure occurred in association with antepartum hemorrhage in 15, postpartum hemorrhage in 10, intrauterine death of fetus in 11, preeclampsia or eclampsia in 9, and septic abortions or puerperal sepsis in 7. Thirty-six patients required dialysis therapy because of moderate to severe azotemia. Renal histology was studied in 12 cases. Acute cortical necrosis was present in 9, extensive tubular necrosis in 2, and 1 patient had membranoproliferative glomerulonephritis. Twenty-two (51%) patients recovered normal renal function, while 11 (26%) developed irreversible renal dysfunction and 10 (23%) expired. Mortality and morbidity in this region is still quite high in obstetrical situations. Poor health infrastructure and lack of antenatal health clinics leads to development of major complications at the time of childbirth, which is mostly conducted at home by untrained personnel in quite a few cities of the country.     

Edema and acute renal failure

Acute renal failure (ARF) with overhydration and edematous state may follow Acute endocapillary proliferative glomerulonephritis and extracapillary glomerulonephritis, because of reduction of the glomerular capillary area available for filtration. But ARF may also be observed in edematous patients with minimal change nephrotic syndrome; it may require dialysis until recovery and is attributable to some of the following factors: (1) ischemic renal injury, (2) hypovolemia, (3) interstitial edema with tubular collapse, (4) redistribution of renal blood flow (RBF) from cortical to juxtaglomerular nephrons, (5) decrease of capillary filtration coefficient (Kf), (6) use of nonsteroidal antiinflammatory drugs. Congestive heart failure also leads to prerenal azotemia and edema formation secondary to salt retention. Multiple organ dysfunction syndrome (MODS) is frequently associated with ARF; but edema occurs even without ARF in septic patients with severe inflammatory response syndrome (SIRS). ARF may follow severe burns; burned patients are frequently edematous because of a rapid leak of fluid from the vascular bed into the wound; edema in undamaged areas occurs in the 'flow phase', because of a fall of oncotic pressure because of massive loss of plasma proteins into the wound. Edema must be treated with diuretics or by dialysis.     

Renal failure in the ICU: comparison of the impact of acute renal failure and end-stage renal disease on ICU outcomes

BACKGROUND: Acute renal failure (ARF) is associated with a persistent high mortality in critically ill patients in intensive care units (ICUs). Most studies to date have focused on patients with established, intrinsic ARF or relatively severe ARF due to multiple factors. None have examined outcomes of dialysis-dependent chronic renal failure [end-stage renal disease (ESRD)] patients in the ICU. We examined the incidence and outcomes of ARF in the ICU using a standard definition and compared these to outcomes of ICU patients with either ESRD or no renal failure. We sought to determine the impact of renal dysfunction and/or loss of organ function on outcome. METHODS: We prospectively scored 1530 admissions to eight ICUs over a 10-month period for illness severity at ICU admission using the Acute Physiological and Chronic Health Evaluation (APACHE III) evaluation tool. Patients were defined as having ARF based on the definition of Hou et al (Am J Med 74:243-248,1983) designed to detect significant measurable declines in renal function based on serum creatinine. ESRD patients were identified as being chronically dialysis-dependent prior to ICU admission and the remainder had no renal failure. Clinical characteristics at ICU admission and ICU and hospital outcomes were compared between the three groups. RESULTS: We identified 254 cases of ARF, 57 cases of ESRD and 1219 cases of no renal failure for an incidence of ARF of 17%. Roughly half the ARF patients had ARF at ICU admission and the remainder developed ARF during their ICU stay. Only 11% of ARF patients required dialysis support. ARF patients had significantly higher acute illness severity scores than those with no renal failure, whereas patients with ESRD had intermediate severity scores. ICU mortality was 23% for patients with ARF, 11% for those with ESRD, and 5% for those with no renal failure. There was no difference in outcome between patients who had ARF at ICU admission and those who developed ARF in the ICU. Patients with ARF severe enough to require dialysis had a mortality of 57%. APACHE III predicted outcome very well in patients with no renal failure and patients with ARF at the time of scoring but underpredicted mortality in those who developed ARF after ICU admission and overestimated mortality in patients with ESRD. CONCLUSIONS: ARF is common in ICU patients and has a persistent negative impact on outcomes, although the majority of ARF is not severe enough to require dialysis support. The mortality of patients with ARF from all causes is almost exactly similar to that noted using the same criteria two decades ago. More profound ARF requiring dialysis continues to have an even greater mortality. Nevertheless, acute declines in renal function are associated with a mortality that is not well explained simply by loss of organ function. The majority of ARF patients who did not require dialysis still had a considerably higher mortality than the ESRD patients, all of whom required dialysis; while ARF patients who did require dialysis had a much higher morality than ESRD patients. APACHE III performs well and captures the mortality of patients with ARF at the time of scoring. Development of ARF after scoring has a profound effect on standardized mortality. We were unable to identify a unique mortality associated with ARF, but the presence of measurable renal insufficiency continues to be a sensitive marker for poor outcome.