Search

Background: Acute kidney injury (AKI) occurs in 10 to 60% of patients with leptospirosis. The aim of this study is to investigate markers for oliguric AKI in leptospirosis., Methods: A retrospective study was performed with 196 consecutive patients with leptospirosis-associated AKI. These patients were categorized into either oliguric or non-oliguric according to their urine output. Clinical and laboratory characteristics were compared between the two groups., Results: Among these patients, 64 (32.6%) were oliguric and 132 (67.4%) nonoliguric. Markers for oliguria were age higher than 40 years (OR = 1.02, p = 0.04), hyponatremia (OR = 0.94, p = 0.03), elevated serum creatinine (OR = 1.11, p = 0.04), low arterial pH (OR = 1.0002, p = 0.01), high levels of AST (OR = 1.005, p = 0.01), crackles (OR = 3.83, p < 0.001) and direct bilirubin (OR = 1.03, p = 0.03). Elevated activated prothrombin time (OR = 0.97, p = 0.03) was a factor associated with nonoliguric AKI. Independent markers for oliguria were crackles (OR = 5.17, p = 0.0016) and direct bilirubin levels (OR = 1.051, p = 0.04). Mortality was significantly higher in oliguric than nonoliguric (27 vs. 8%, p < 0.001). Renal function at discharge was similar in oliguric and nonoliguric patients., Conclusion: Age higher than 40 years, hyponatremia, elevated serum creatinine, low arterial pH, high levels of AST, crackles and direct bilirubin levels would be useful to early identify patients with oliguric AKI in leptospirosis., (Copyright 2009 S. Karger AG, Basel.)

Rhabdomyolysis is associated with infectious diseases in approximately 5% of cases and acute kidney injury occurs in 33-50% of cases. Gangrenous myositis is a deep seated infection of the subcutaneous and muscular tissues. We report the case of an 18 year-old man who was admitted to the emergency room with leg pain, fever, nausea, vomiting and oliguria. Physical examination showed moderate dehydration, peripheral cyanosis and skin necrosis with severe myalgia and no subcutaneous gas. Laboratory findings at admission were: serum urea 111 mg/dL, creatinine 1.3 mg/dL, potassium 6.3 mEq/L, creatine kinase (CK) 112,452 IU/L, aspartate amino transaminase (AST) 1116 IU/L, alanine amino transaminase (ALT) 1841 IU/L, pH 7.31, bicarbonate (HCO3) 11 mEq/L and lactate 4.3 mmol/L. Emergency hemodyalisis was started, and antibiotics were given due to high suspicion for bacterial infection. The patient developed respiratory insufficiency and septic shock needing mechanical ventilation and vasoactive drugs. He presented spontaneous gangrenous myositis in both legs and in his left arm. After 26 sessions of hemodialysis, partial recovery of renal function was observed. He was discharged from the ICU after 38 days, still with leg pain. Acute kidney injury due to rhabdomyolysis should be considered as a possible complication of gangrenous myositis.

Background: Obstructive nephropathy decreases renal blood flow (RBF) and glomerular filtration rate (GFR), causing tubular abnormalities, such as urinary concentrating defect, as well as increasing oxidative stress. This study aimed to evaluate the effects of N-acetylcysteine (NAC) on renal function, as well as on the protein expression of aquaporin 2 (AQP2) and endothelial nitric oxide synthase (eNOS), after the relief of bilateral ureteral obstruction (BUO)., Methods: Adult male Wistar rats were divided into four groups: sham (sham operated); sham operated + 440 mg/kg body weight (BW) of NAC daily in drinking water, started 2 days before and maintained until 48 h after the surgery; BUO (24-h BUO only); BUO + NAC-pre (24-h BUO plus 440 mg/kg BW of NAC daily in drinking water started 2 days before BUO); and BUO + NAC-post (24-h BUO plus 440 mg/kg BW of NAC daily in drinking water started on the day of BUO relief). Experiments were conducted 48 h after BUO relief., Results: Serum levels of thiobarbituric reactive substances, which are markers of lipid peroxidation, were significantly lower in NAC-treated rats than in the BUO group rats. The administration of NAC provided significant protection against post-BUO GFR drops and reductions in RBF. Renal cortices and BUO rats presented decreased eNOS protein expression of eNOS in the renal cortex of BUO group rats, whereas it was partially recovered in BUO + NAC-pre group rats. Urine osmolality was significantly lower in BUO rats than in sham group rats or NAC-treated rats, the last also presenting less interstitial fibrosis. Post-BUO downregulation of AQP2 protein expression was averted in the BUO + NAC-pre group rats., Conclusions: This study demonstrates that NAC administration ameliorates the renal function impairment observed 48 h after the relief of 24-h BUO. Oxidative stress is important for the suppression of GFR, RBF, tissue AQP2 and eNOS in the polyuric phase after the release of BUO.

Tenofovir disoproxil fumarate (TDF) is a first-line drug used in patients with highly active retroviral disease; however, it can cause renal failure associated with many tubular anomalies that may be due to down regulation of a variety of ion transporters. Because rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist induces the expression of many of these same transporters, we tested if the nephrotoxicity can be ameliorated by its use. High doses of TDF caused severe renal failure in rats accompanied by a reduction in endothelial nitric-oxide synthase and intense renal vasoconstriction; all of which were significantly improved by rosiglitazone treatment. Low-dose TDF did not alter glomerular filtration rate but produced significant phosphaturia, proximal tubular acidosis, polyuria and a reduced urinary concentrating ability. These alterations were caused by specific downregulation of the sodium-phosphorus cotransporter, sodium/hydrogen exchanger 3 and aquaporin 2. A Fanconi's-like syndrome was ruled out as there was no proteinuria or glycosuria. Rosiglitazone reversed TDF-induced tubular nephrotoxicity, normalized urinary biochemical parameters and membrane transporter protein expression. These studies suggest that rosiglitazone treatment might be useful in patients presenting with TFV-induced nephrotoxicity especially in those with hypophosphatemia or reduced glomerular filtration rate.

Background: To compare estimated glomerular filtration rate (GFR) by Schwartz formula and cystatin C-derived formula in a large population of children with a large spectrum of renal disease., Methods: Serum creatinine, cystatin C and estimated GFR were determined in 273 children, 254 with renal disease, and a mean age of 10.0+/-4.4 y. Nineteen children were used as control, with a mean age of 8.5+/-4.2 y., Results: The children had nephrotic syndrome (16.5%), glomerulonephritis (11.4%), neurogenic bladder (11.4%), hydronephrosis (9.8%), asymptomatic hematuria (11%), chronic renal disease (5.9%) and other diseases (11%). Cystatin C, creatinine, Schwartz estimated GFR and cystatin C estimated GFR (mean+/-SD) were 1.30+/-1.03 mg/dl, 0.82+/-1.20 mg/l, 143+/-72 ml/min/1.73 m(2) and 88+/-36 ml/min/1.73 m(2), respectively. Although GFR estimated by creatinine and cystatin C had a significant correlation, the Bland-Altman analysis showed greater differences between GFR estimated by the 2 methods, with a mean difference of 50 ml/min. Besides, >50% of the patients with a reduced cystatin C estimated GFR had a normal GFR when analyzed by the Schwartz formula., Conclusions: Our data shows that cystatin C-based GFR is more sensitive than previous study had demonstrated. It is important to perform studies in specific populations to determine the variability in GFR measurements.

Background: Acute kidney injury (AKI) is a common complication in many infectious diseases. There are few studies to investigate risk factors for death in infectious diseases-associated AKI., Methods: This is a retrospective study including all patients with acute kidney injury (AKI) admitted to an infectious diseases intensive care unit (ICU) in Brazil between October 2003 and September 2006., Results: A total of 722 patients were admitted to the infectious disease ICU in the study period. AKI occurred in 147 cases (17.7%). The mean age was 45 +/- 5.6 years, and 77% were male. The mean length of hospital stay was 11.5 +/- 10.3 days. The main causes of ICU hospitalization were acquired immunodeficiency syndrome (AIDS)-related diseases (28 .6%), pneumonia 13%), leptospirosis (11.6%), meningitis (8.2%), disseminated histoplasmosis (6.8%) and tetanus (5.4%). The main cause of AKI was sepsis (41.5%). Patients were classified according to RIFLE as "Risk" (5.6%), "Injury" (21.7%) and "Failure" (72.7%). Patients in "Failure" showed a higher mortality (p = 0.007). Multivariate analysis showed that dependent risk factors for death were oliguria (OR = 5.59, P = 0.002), metabolic acidosis (OR = 5.13, P = 0.01), sepsis (OR = 4.79, P = 0.001), hypovolaemia (OR = 4.11, P = 0.01), use of vasoactive drugs (OR = 3.34, P = 0.02), use of mechanical ventilation (OR = 2.94, P = 0.03) and high APACHE II score (OR = 1.14, P = 0.001)., Conclusion: There are important risk factors for death among critically ill patients with infectious diseases associated with AKI.

The aims of this study were to determine whether standard base excess (SBE) is a useful diagnostic tool for metabolic acidosis, whether metabolic acidosis is clinically relevant in daily evaluation of critically ill patients, and to identify the most robust acid-base determinants of SBE. Thirty-one critically ill patients were enrolled. Arterial blood samples were drawn at admission and 24 h later. SBE, as calculated by Van Slyke's (SBE VS) or Wooten's (SBE W) equations, accurately diagnosed metabolic acidosis (AUC = 0.867, 95%CI = 0.690-1.043 and AUC = 0.817, 95%CI = 0.634-0.999, respectively). SBE VS was weakly correlated with total SOFA (r = -0.454, P < 0.001) and was similar to SBE W (r = -0.482, P < 0.001). All acid-base variables were categorized as SBE VS <-2 mEq/L or SBE VS <-5 mEq/L. SBE VS <-2 mEq/L was better able to identify strong ion gap acidosis than SBE VS <-5 mEq/L; there were no significant differences regarding other variables. To demonstrate unmeasured anions, anion gap (AG) corrected for albumin (AG A) was superior to AG corrected for albumin and phosphate (AG A+P) when strong ion gap was used as the standard method. Mathematical modeling showed that albumin level, apparent strong ion difference, AG A, and lactate concentration explained SBE VS variations with an R(2) = 0.954. SBE VS with a cut-off value of <-2 mEq/L was the best tool to diagnose clinically relevant metabolic acidosis. To analyze the components of SBE VS shifts at the bedside, AG A, apparent strong ion difference, albumin level, and lactate concentration are easily measurable variables that best represent the partitioning of acid-base derangements.

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 >or= 90 mL/min/1.73 m(2)) and partial recovery (GFR < 90 mL/min/1.73 m(2)). Only 39% of the patients achieved complete recovery. Patients with partial recovery achieved their maximal GFR (63 +/- 9 mL/min/1.73 m(2)) 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.

Background: Results from a number of studies suggest that the delayed manifestation of acute kidney injury (AKI) is associated with higher in-hospital mortality, while other studies were unable to demonstrate any difference among early and delayed AKI in terms of in-hospital mortality., Objective: The aim of this study was to investigate differences in outcome among patients with AKI upon admission to an intensive care unit (ICU) and those who develop AKI post-admission., Methods: We studied patients with AKI secondary to infectious diseases admitted to the ICU. We retrospectively compared data on patients admitted with AKI (early AKI) with data on those who developed AKI 24 h after admission (delayed AKI)., Results: Acute kidney injury occurred in 147 of 829 (17.7%) patients admitted to the ICU. Of these, 96 (65%) had early AKI and 51 (35%) had delayed AKI. Renal failure was classified according to RIFLE criteria-an AKI-specific severity score that is used to place patients into one of five categories: risk, injury, failure, loss or end-stage renal disease. Based on these criteria, 6% of the early AKI and 4% of the delayed AKI patients were in risk category, 18% of the early AKI and 27% of the delayed AKI patients were in the injury category and 76% of the early AKI and 69% of the delayed AKI patients were in the failure category. We found no significant association between RIFLE and death. On admission, patients with early AKI had statistically significantly higher serum urea and creatinine levels than delayed AKI patients (P<0.0001). Arterial bicarbonate was lower in early AKI (P=0.02). Sepsis, hypotension and use of mechanical ventilation were more frequent in delayed AKI (P<0.05). The APACHE II score was higher in early AKI (P=0.05) patients. In total, 98 (66.7%) patients died, with a tendency towards higher mortality in patients with delayed AKI (61.5 vs. 76.5%, P=0.07)., Conclusion: Mortality among patients with infectious diseases-associated AKI admitted to the ICU is high, with a trend to be higher in those who developed delayed AKI.

Acidosis is a common and deleterious aspect of maintenance dialysis. Traditionally, it is considered to be an elevated anion gap acidosis caused by the inability to excrete nonvolatile anions. Stewart's approach made it possible to identify real determinants of the acid-base status and allowed quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to identify and quantify each component of acidosis in hemodialysis maintenance patients. Sixty-four maintenance hemodialysis patients and 14 controls were enrolled in this study. Gasometrical and biochemical analysis were performed before the midweek dialysis session. Quantitative physicochemical analysis was carried out using the Stewart methodology. Hemodialysis patients were found to have mild acidemia (mean pH: 7.33 +/- 0.06 versus 7.41 +/- 0.05) secondary to metabolic acidosis (serum bicarbonate: 18.8 +/- 0.26 versus 25.2 +/- 0.48 mEq/l). The metabolic acidosis was due to retention of unmeasured anions (6.5 +/- 0.29 versus 3.1 +/- 0.62 mEq/l), hyperchloremia (105.1 +/- 0.5 versus 101.8 +/- 0.7 mEq/l), and hyperphosphatemia (5.90 +/- 0.19 versus 3.66 +/- 0.14 mg/dl). Compared with control values, the unmeasured anions and hyperchloremia had a similar acidifying effect (3.4 and 3.3 mEq/l), corresponding to almost 90% of the metabolic acidosis. Unmeasured anions and hyperchloremia are important components of acidosis in maintenance hemodialysis, in addition to phosphorus. Future studies to determine the etiology and consequences of hyperchloremic acidosis are warranted.

Background: Renal abnormalities in leprosy have been largely described in medical literature, but there are few studies evaluating renal function in these patients., Methods: This is a cross-sectional study in 59 consecutive paucibacillary (PB) and multibacillary (MB) leprosy patients. Glomerular filtration rate (GFR) was estimated by simplified-MDRD formula. Microalbuminuria was determined by 24 h urine collection. Urinary acidification capacity was measured after water deprivation and acid-loading with CaCl(2). Urinary concentration capacity was evaluated after desmopressin acetate administration, using the urinary to plasma osmolality (U/P(osm)) ratio. All parameters except microalbuminuria were measured in a control group of 18 healthy volunteers., Results: Age and gender were similar between leprosy (MB or PB) and control groups. GFR 1.2 mg/dl was observed in 17.9% of MB patients and in none of the controls (P=0.020). A negative correlation was observed between GFR and time of treatment (r= -0.339; P=0.002). Age and time of treatment were independent risk factors for GFR

Background: Many factors are involved in the progression of secondary hyperparathyroidism, including acidosis. Stewart's approach has made it possible to identify real determinants of acid-base status, making chloride a real etiological factor of acid-base disturbances. In addition, it has allowed the quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to quantify each component of acidosis in hemodialysis patients and correlate them with renal bone disease biochemical markers., Methods: Sixty maintenance hemodialysis patients and 14 controls were enrolled in this study. Each acid-base determinant was quantified and correlated in multivariate regression with intact serum parathormone and bone-specific alkaline phosphatase, adjusting to other variables., Results: Hemodialysis patients were more acidotic than controls, mainly due to the retention of unmeasured anions, hyperchloremia and hyperphosphatemia. In multivariate regression analysis, the only acid-base determinants independently correlated with bone markers were chloride, calcium and phosphorus (beta=0.537, beta=-0.256 and beta=-0.242, respectively). Although unmeasured anions were a major component of acidosis, they had no correlation with these markers., Conclusion: Although unmeasured anions are considered the main component of acidosis in hemodialysis patients, serum chloride was the only acid-base determinant correlated with bone markers.

Background: Metabolic acidosis is highly prevalent in critically ill patients with acute renal failure. Little is known about the mechanisms by which renal replacement therapy intervenes in such cases. The objective of this study is to analyze the role of hemodialysis in acidosis correction in intensive care unit patients, with an emphasis on chloride levels in plasma and dialysate., Methods: We studied 19 intermittent hemodialysis procedures in 17 acidotic patients. The patients were grouped by procedure type (conventional or sustained low-efficiency dialysis) and by predialysis plasma chloride level (higher or lower than the dialysate chloride concentration). Immediately before and after each procedure, blood samples were collected for biochemical analysis. The Stewart method was used to calculate the strong ion difference and strong ion gap., Results: The patients presented acidosis related to hyperchloremia, hyperphosphatemia, and high unmeasured anions. Hypoalbuminemia had an alkalinizing effect. Hemodialysis corrected acidosis mainly by reducing phosphate and unmeasured anions. In the group as a whole, chloride levels did not change after dialysis. However, when analyzed according to predialysis plasma chloride, the high-chloride group presented a reduction in plasma chloride, resulting in better base excess improvement (Delta standard base excess) than in the low-chloride group. Among the determinants of acid-base status, the only factors correlating with Delta SBE were Delta strong ion gap and Delta chloride., Conclusion: The serum chloride/dialysate chloride relationship during hemodialysis has an important impact on acidosis control.

Malignant hypertension is a well-defined condition associated with high blood pressure and acute target-organ damage. Although 95% of cases are secondary to essential hypertension, its etiological profile is broad. Juxtaglomerular cell tumor is a rare condition, with only approximately 65 cases reported to date. We describe a patient with malignant hypertension with acute renal failure and intestinal ischemia secondary to a juxtaglomerular cell tumor. We believe this is the first case of juxtaglomerular cell tumor causing malignant hypertension. The diagnostic approach and treatment are discussed.