Course Of Acute Renal Failure Research Articles

Persistent Aseptic Pyelonephritis After Acute Bacterial Pyelonephritis: Possible Role of Corticosteroids

Persistent Aseptic Pyelonephritis After Acute Bacterial Pyelonephritis: Possible Role of Corticosteroids

Influence of preliminary introduction of placenta cryoextracts on ultrastructure of rat’s adrenal gland glomerular zone with acute renal failure.

Background. When developing new available methods of restorative correction of renal function in renal insufficiency, the placenta preparations are increasingly used. The course of acute renal failure and its transformation into a chronic form significantly affects aldosterone, that is one of the links of the hypothalamic-pituitary-adrenal system. Determination of ultrastructural adrenocorticocyte changes in the glomerular zone of adrenal glands and the level of saturation of cells with lipids will allow judging the degree of this hormone secretion. The objective of the research was to investigate the ultrastructure of cells of adrenal cortex glomerular of rats with acute renal failure when introducing the placenta cryoextracts of allogeneic and xenogeneic origin prior to the renal pathology simulation. Methods. The research object were 65 white male rats aged 4 months. Animals were givenwith the cryoextracts of placental tissue of various origins by 0.5 ml three times a week. A week after the introduction of cryoextracts, renal insufficiency was modeled by intramuscular injection of 50% aqueous solution of glycerol in a dose of 10 ml per 1 kg body weight. Animals were divided into 3 groups: 1 - rats with the simulated renal failure; 2, 3 - rats with simulated renal failure, which were pre-administered with cryoexracts of the rat and human placenta, respectively. Animals were withdrawn from the experiment to the first, second and third week after the introduction of glycerol. The ultrastructure of the cells was examined using an electron microscope PEM-125K (Selmi JSC). Results. Within 3 weeks of glycerol model of an acute renal failure, regardless of the previous administration of either rat’s or human placenta cryoextracts the ultrastructure of adrenocorticocytes of glomerular zone showed the signs of strengthening steroidogenesis, which were manifested by hypertrophy of endoplasmic reticulum and mitochondria, swelling of mitochondria, formation of myelin-like structures and mitochondrial vacuoles as well as tight mitochondrial complexes, endoplasmic reticulum and liposomes. Conclusion. The signs of increased steroidogenesis in glomerular zone of rat’s adrenal cortex were most pronounced when introducing the xenogeneous cryoextracts of placenta prior to the start of pathology modeling.

Old World hantaviruses: Aspects of pathogenesis and clinical course of acute renal failure

Hantavirus-associated diseases represent emerging infections that are ranked in the highest priority group of communicable diseases for surveillance and epidemiological research. In the last years, several novel hantavirus species were described and the number of host reservoir species harboring hantaviruses is also increasing. Reports of cases with severe or atypical clinical courses become also more frequent. These facts raise more and more questions concerning host reservoir specificity, pathogenicity and molecular mechanism of pathogenesis. Hantavirus disease is characterized by vascular leakage due to increased capillary permeability. The infection manifests often in the lung (hantaviral cardiopulmonary syndrome; HCPS) or in the kidney (hemorrhagic fever with renal syndrome, HFRS). The underlying mechanisms of both syndromes are probably similar despite the difference in organ tropism. Characterization of hantaviral replication cycle and of patient-specific determinants will help to identify factors responsible for the clinical symptoms and course.

Prevention of Contrast‐Induced Nephropathy in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention: A Systematic Review

To evaluate the current prophylactic strategies against CIN in patients with STEMI treated by primary percutaneous coronary intervention. Contrast-induced nephropathy (CIN) is the third leading course of acute renal failure and a recognized complication to cardiac catheterization. CIN is associated with increased risk of cardiac adverse events and mortality, and recent studies point at the risk of developing a transient or persistent renal dysfunction. Patients with ST-elevation myocardial infarction treated by primary percutaneous coronary intervention have a markedly increased risk of developing CIN. At present no strategy is universally accepted in the prevention of CIN in the acute setting of primary percutaneous coronary intervention. We performed a systematic search in Pubmed and EMBASE and ended up including nine randomised clinical trials; six studies of N-acetylcysteine, one study of early and late hydration regimens, one study of recombinant human brain natriuretic peptide and one study comparing a low-osmolar contrast agent with an iso-osmolar contrast agent. Recombinant human brain natriuretic peptide and the regimens of hydration significantly reduced the incidence of CIN and administration of N-acetylcysteine in one of the six studies significantly reduced the occurrence of CIN. The iso-osmolar contrast agent was not proven to be superior to the low-osmolar contrast agent in terms of preventing CIN. Preliminary studies are promising but further studies are needed before any prevention strategy against CIN can be recommended in routine care of patients undergoing primary percutaneous coronary intervention for STEMI.

TEMPOL IMPROVES REGIONAL HEMODYNAMICS IN SPONTANEOUSLY HYPERTENSIVE RATS WITH ACUTE RENAL FAILURE: 3C.06

Objective: Acute renal failure (ARF) and hypertension as a comorbid disorders can be found frequently in intensive care unit patients. The aim of our study was to investigate the antihypertensive effects of 4-Hydroxy-2, 2, 6, 6-tetramethylpiperidine-N-oxyl (tempol), synthetic SOD mimetic, on regional haemodynamics in the course of ARF in hypertension. Design and Method: Experiment was performed in anesthetized, six-month-old male spontaneously hypertensive rats (SHR). The right kidney was removed and ARF was induced by clamping the left renal artery for 40 minutes. SHR were divided in 3 experimental groups: sham operated group (SHAM; n = 7); ARF group (ARF; n = 9); and ARF group with tempol treatment (40 mg/kg/h) (ARF+TEM; n = 8). Tempol was given by infusion during the period of three hours after reperfusion. Mean arterial pressure (MAP), carotid blood flow (CBF) and renal blood flow (RBF) were measured and carotid vascular resistance (CVR) and renal vascular resistance (RVR) was calculated 24 h after reperfusion.Conclusion: Our results indicate that in hypertension free oxygen species contribute to renal vasoconstiction, one of the major pathophysiological mechanism of postischemic ARF.

The role of hypotension in the development of acute renal failure

Acute renal failure in critically ill patients is common and is associated with high morbidity and mortality rates [1]. When defined as a serum creatinine of 300 μmol/l (3.5 mg/dl) or more and/or a urine output of <500 ml/day, acute renal failure was shown to affect almost 25% of patients in the ICU [2]. Using the RIFLE criteria, studies have reported that between 10 and 67% of ICU patients have acute kidney injury [3]. Moreover, by increasing the hospital length of stay [2,4,5] and by inducing the need for renal replacement therapy, acute renal failure has substantial economic consequences [5,6]. Acute renal failure is typically multifactorial. The classical classification of renal diseases seen in any nephrology textbook does not apply to the vast majority of critically ill patients, who usually develop what is called ‘acute tubular necrosis’, even though the term is a misnomer as few of the tubular cells are actually necrotic [7]. The typical course of acute renal failure in a severely ill patient involves several factors including sepsis with hypovolaemia, (possibly transient) hypotension and administration of nephrotoxic therapeutic agents and/or contrast material, in a patient with co-morbidities such as diabetes and arteriosclerosis [2,8]. In this issue of Nephrology Dialysis and Transplantation, Liu and co-workers report that development of acute renal failure is usually preceded by an episode of relative hypotension [9]. The authors retrospectively selected two cohorts of patients, one with acute kidney injury as defined by the RIFLE criteria and one without. Blood pressure readings were obtained for 3 days prior to the development of acute kidney injury and for a similar 3-day period in patients without renal failure, and compared to baseline values

Acute Renal Failure in Critically Ill Surgical Patients: Persistent Lethality Despite New Modes of Renal Replacement Therapy

Despite improved resuscitation and sepsis care, acute renal failure (ARF) remains common in critically ill surgical patients. New methods of renal replacement therapy (RRT) are being used in surgical intensive care units (SICUs), including high-flux hemodialysis (HD) and continuous RRT (CRRT). RRT is being used increasingly early in the course of ARF, but data are scant to suggest that mortality is improved. Consequently, we determined whether outcomes were improved with CRRT in SICU patients, and hypothesized that CRRT lowers mortality for patients with ARF. Patients who developed ARF (acute increase in serum creatinine concentration >or=2.4 mg/dL) in the SICU from 1993 to 2004 were identified. Data collected prospectively included year of admission, age, gender, Acute Physiology and Chronic Health Evaluation (APACHE) III score, cumulative multiple organ dysfunction score and its individual components, cumulative nonrenal organ dysfunction score, and need for RRT. Patients were stratified January 1994 to January 2001 (pre-CRRT) and February 2001 to December 2004 (post-CRRT). The primary endpoint was mortality. Among 8,505 SICU patients, 530 (6.2%) developed ARF. Three hundred and eleven patients were treated pre-CRRT and 219 thereafter. Female patients comprised 35% of ARF patients. The mean age was 69 years +/- 2 years, and the mean APACHE III score was 81 +/- 1 point for ARF patients. HD was performed in 15.6% of ARF patients before 2001 and 5.5% of ARF patients in 2001 and thereafter. CRRT was performed in 20.1% of ARF patients in 2001 and thereafter. Overall mortality for ARF patients was 45% (APACHE III normative predicted mortality: 55%) with no difference over time (pre-CRRT = 46.3%, post-CRRT = 45.2%, p = 0.86). Patients who required RRT had a mean APACHE III score of 91 +/- 1 point, with 61% mortality (predicted mortality: 67%), with no difference over time. Independent predictors of mortality overall and for ARF patients included age and the magnitude of renal, cardiovascular, hepatic, and neurologic dysfunction. In comparison with CRRT, HD was associated with a decreased risk of death. Despite more frequent RRT and the use of CRRT, the mortality of ARF in critically ill surgical patients remains high because of nonrenal organ dysfunction. Considering that ARF-related mortality was decreased by intermittent HD, and that intermittent RRT is less costly, patients who need RRT should be treated preferentially with HD.

Malaria-induced renal damage: facts and myths

Malaria infections repeatedly have been reported to induce nephrotic syndrome and acute renal failure. Questions have been raised whether the association of a nephrotic syndrome with quartan malaria was only coincidental, and whether the acute renal failure was a specific or unspecific consequence of Plasmodium falciparum infection. This review attempts to answer questions about "chronic quartan malaria nephropathy" and "acute falciparum malaria nephropathy". The literature review was performed on all publications on kidney involvement in human and experimental malarial infections accessible in PubMed or available at the library of the London School of Hygiene and Tropical Medicine. The association of a nephrotic syndrome with quartan malaria was mostly described before 1975 in children and rarely in adult patients living in areas endemic for Plasmodium malariae. The pooled data on malaria-induced acute renal failure included children and adults acquiring falciparum malaria in endemic areas either as natives or as travellers from non-tropical countries. Non-immunes (not living in endemic areas) had a higher risk of developing acute renal failure than semi-immunes (living in endemic areas). Children with cerebral malaria had a higher rate and more severe course of acute renal failure than children with mild malaria. Today, there is no evidence of a dominant role of steroid-resistant and chronic "malarial glomerulopathies" in children with a nephrotic syndrome in Africa. Acute renal failure was a frequent and serious complication of falciparum malaria in non-immune adults. However, recently it has been reported more often in semi-immune African children with associated morbidity and mortality.

Rolle des L-Arginin/NO-Stoffwechselweges im akuten Nierenversagen

Role of the L-arginine/NO-pathway in acute renal failure ■ Summary Regulation of renal hemodynamics – in particular intraglomerluar hemodynamics -is closely related to the L-arginine/ NO-pathway. Almost all forms of acute renal failure (ARF) are characterized by a reduction in renal plasma flow (RPF) and increased renal vascular resistance. NO, metabolized from L-arginine, is capable of improving renal function due to its vasorelaxing properties in almost all models of ARF, whereas unselective inhibition of nitric oxide synthase (NOS) generally exerts contrary effects. Increased tubular generation of oxygen radicals in the early course of ischemic ARF indicates increased oxidative stress. Simultaneously regulatory changes in expression of iNOS (inducible NOS) and eNOS (endothelial NOS) are observed. Apart from the positive functional effects with L-arginine supplementation a remarkable reduction in the formation of oxygen radicals and reduced overexpression of iNOS are observed. This is important, because in ischemic ARF increased expression of iNOS is accompanied by increased formation of oxygen radicals and peroxynitrite. Both substances are highly reactive and exert many cytotoxic effects. eNOS-derived NO probably plays such an important role in maintaining and improving renal and intraglomerular hemodynamics that negative effects from iNOS-derived NO are overcome. The roles of NOS are different for different types of NOS and also depend on the time course of ARF. Future management strategies should focus on the interplay between antioxidants and NO regulators and the correlation of reactive oxygen species and NO.

Fractional excretion of urea in the follow-up of acute renal failure due to prerenal azotemia

Fractional excretion of urea (FEU) is a major issue to discriminate between prerenal azotemia and acute tubular necrosis in acute renal failure (ARF). Its role in the course of ARF remains unclear. The aim of this study was to evaluate FEU in the follow-up of ARF due to prerenal azotemia in order to predict the necessity of renal replacement therapy (RRT). The prospective study took place at the ICU of Stadtspital Waid, Zurich. All patients admitted starting from 19 February 2006 were evaluated for ARF according to the RIFLE classification. ARF due to prerenal azotemia was defined as ARF combined with FEU of less than or equal to 35%. FEU was calculated as [(urine urea/blood urea)/(urine creatinine/plasma creatinine)] × 100. Urine specimens were taken and FEU was calculated daily until complete or partial renal recovery was reached or the criteria for RRT were met. The goal of therapy was reconstitution of renal function by treatment of the underlying condition. RRT was initiated according to the usual criteria. Statistics were determined using Fisher's exact test. By 7 December 2006, 15 patients met the inclusion criteria for ARF due to prerenal azotemia (nine males, six females). The mean age was 71 ± 11 (SD) years for male patients and 58 ± 31 years for female patients. Twelve out of the 15 patients responded to conservative management and had complete or partial renal recovery. Three patients needed RRT. Two of them refused RRT and died during the course of the disease. During the first 48 hours after initiation of conservative therapy, FEU remains less than or equal to 35% in all three patients who needed RRT. By contrast, nine out of 12 patients in whom renal function recovered without RRT showed a FEU of more than 35% within the first 48 hours (P < 0.05) (Figure ​(Figure11). Figure 1 Fractional excretion of urea (FEU) in the follow-up of acute renal failure (ARF) due to prerenal azotemia. Data presented as mean ± SD. n = number of patients. In patients presenting with ARF due to prerenal azotemia, an increase of FEU above 35% within the first 48 hours after initiation of conservative therapy for ARF is a valuable parameter to predict renal recovery. After initiation of conservative therapy, measurement of FEU is of no value concerning discrimination of prerenal azotemia and acute tubular necrosis in ARF.

Leptospiral Acute Renal Failure: Effects of Dopamine and Furosemide

From unpublished experience of clinicians in the rural tropics, the combination of furosemide and dopamine is beneficial in the management of mild acute renal failure in tropical disease. We studied two groups of patients with leptospirosis and mild acute renal failure whose serum creatinine ranged from 2.4 to 5 mg/dL and fractional excretion of sodium varied from 1.21 to 2.08%. Group 1, consisting of 9 patients with the serum creatinine ranging from 2.4 to 5 mg/dL, served as the control. They received only penicillin G sodium and supportive treatment. Group 2, consisting of 8 patients with the serum creatinine ranging from 2.8 to 5 mg/dL, received, in addition to penicillin, dopamine (renal dose) and furosemide along with fluid and electrolyte replacement. The control group ran the usual clinical course of acute renal failure, and 3 patients required dialysis. There was profuse diuresis, and the recovery of renal function was faster in group 2 patients. Dopamine and furosemide are therefore useful in mild acute renal failure in leptospirosis. It is felt that this combination could be beneficial in the management of mild acute ischemic renal failure due to a clean single insult.

Mitral valve surgery and acute renal failure

Mitral valve surgery and acute renal failure

Low-Dose Dopamine: A Physiologically Based Review

In an attempt to prevent or alter the course of acute renal failure, many surgeons continue to use low-dose dopamine. This article critically reviews the physiologic reasons why low-dose dopamine is not clinically efficacious. A critical review of English language literature. The effect of dopamine on renal blood flow remains controversial. If dopamine does increase renal blood flow, the vascular anatomy of the kidney would limit its effectiveness. Rather than improving renal function, dopamine has been shown to impair renal oxygen kinetics, inhibit feedback systems that protect the kidney from ischemia, and may worsen tubular injury. Dopamine has not been proven useful in the prevention or alteration of the course of acute renal failure as a result of heart failure, cardiac surgery, abdominal aortic surgery, sepsis, and transplantation. Dopamine has been associated with multiple complications involving the cardiovascular, pulmonary, gastrointestinal, endocrine, and immune systems. Based on the anatomy and physiology of the kidney, low-dose dopamine would not be expected to improve renal failure and this has been demonstrated by the lack of efficacy in clinical trials.

Functional aftereffects of intraparenchymatous injection of human fetal stem and progenitor cells to rats with chronic and acute renal failure

Chronic renal insufficiency was modeled in rats by unilateral nephrectomy and electrocoagulation of both poles of the remaining kidney; acute renal failure was induced by 90-min clamping of the vascular pedicle of the only kidney. Injection of unfractionated culture of human fetal kidney cells or bone marrow mesenchymal stem cells into damaged kidney restored its function in rats with chronic renal insufficiency (observation period up to 2 months). After 2.5 months a relapse of chronic renal insufficiency was observed in 1 of 3 rats receiving human fetal kidney cells and in 1 of 2 animals receiving bone marrow mesenchymal stem cell culture. Injection of bone marrow mesenchymal stem cell culture to rats with acute renal failure improved recovery of renal function and prevented the death from uremia, while injection of total culture of human fetal kidney cells had virtually no effect on the course of acute renal failure.

Acute Renal Failure in Dogs After the Ingestion of Grapes or Raisins: A Retrospective Evaluation of 43 Dogs (1992-2002)

A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium × phosphorus product (Ca × P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca × P, and peak Ca × P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.

Paracrine and differentiation mechanisms underlying stem cell therapy for the damaged kidney

NATIVE KIDNEY ACUTE RENAL FAILURE (ARF) occurs in 2‐5% of hospitalized patients and is associated with high mortality (11). Allograft ARF occurs in 30‐50% of deceased donor kidney transplants and leads to longer hospital stays, a higher incidence of acute rejection, and reduced long-term graft survival (13). There is no specific therapy for ARF except for supportive care. A surge of evidence over the last decade supports an important role for inflammatory mediators, microvascular dysfunction, and apoptosis in the pathogenesis of the injury and extension phase of ARF (12). The mechanisms of recovery, less well understood, are felt to include a recapitulation of mechanisms originally involved in renal development. It is commonly believed that kidney progenitor cells, from either the kidney or an extrarenal source, repopulate the kidney during the recovery phase of ARF and drive the repair process (9). A popular model was that damaged/dead cells are removed and the kidney stem cells migrate to necrotic areas, differentiate, and repopulate the kidney. Indeed, injured human kidney transplants from female donors into male recipients were found to have Y chromosome staining of tubular epithelial cells, demonstrating that they were of recipient origin (5). In support of this model are studies in mice in which labeled bone marrow was tracked with -galactosidase (-gal) staining into postischemic kidney. -Gal staining was observed in 20% of the proximal tubular cells at 1 wk after ischemia, and also to some extent within 48 h of ischemia (7). Despite the focus on stem cell effects on repair, mice without functional bone marrow in that study had a worse early course of ARF, suggesting that bone marrow-derived cells had an early protective effect on the injury process. In another murine study, male-derived cells were found in female mouse kidney recipients after ischemia (8). However, recent work has shown that -gal staining to identify differentiated stem cells has considerable limitations, false positive results can result from the kidney’s endogenous -gal, and the staining validity is vulnerable to slight pH shifts (3). In a cisplatin model of ARF, administration of mesenchymal stem cells improved kidney function and structure (10). Given that Y chromosome-containing cells were found in recipient tubular epithelium of female mice and expressed specific lectin-binding proteins found in proximal tubules, transdifferentiation was concluded to be the mechanism of enhanced repair. Administration of skeletal muscle-derived stem cells that were differentiated into endothelial cells provided early protection from ischemic ARF in mice and were detected in glomeruli and peritubular capillaries using green fluorescent protein detection (1).

Prognostic Value of Acute Physiology and Chronic Health Evaluation II and Organ System Failure in Patients with Acute Renal Failure Requiring Dialysis

Background. Despite advances in modern technology of dialysis, prognosis of patients with acute renal failure (ARF) remains poor. To give the clinicians the most useful information, a model that accurately predicts outcome early in the course of ARF is required. However, because ARF is a heterogeneous syndrome and occurs in patients with diverse etiologies and some coexisting diseases, predicting outcome early is hard. The aim of this study is to evaluate prospectively the Acute Physiology and Chronic Health Evaluation (APACHE II) and organ system failure (OSF) models, evaluated prior to dialysis, in predicting hospital mortality. Methods. From June 2002 to March 2004, ARF patients requiring dialysis at Chang Gung Memorial Hospital, Chiayi, were prospectively recruited for this study. The worst clinical and laboratory data in the 24 hours before initiation of dialysis were prospectively evaluated, and the patients' APACHE II score and OSF number were assessed. Results. A total of 61 patients (40 male and 21 female) were enrolled, of whom 38 (62.3%) died before discharge. By multivariate logistic regression, the APACHE II score (odds ratio 1.3 per increase in one score; P< 0.001), or OSF number (odds ratio 1.9 per increase in one OSF; P< 0.01) and oliguria (odds ratio 4.2; P = 0.04), were found to be statistically significant prognostic factors for hospital mortality. Mortality increased progressively and significantly as OSF number (chi-square for trend; P = 0.001) or the APACHE II score (chi-square for trend; P< 0.001) increased. By using Youden's index, the best cut-off value for APACHE II was 24, with 63% sensitivity and 96% specificity. The best cut-off value for OSF number was 2, with a sensitivity of 81.6% and a specificity of 60.9%. The areas under the receiver operating characteristic curves for APACHE II and OSF number were 0.847 (95% confidence interval (CI)= 0.752–0.942; P< 0.01) and 0.769 (95% CI = 0.646–892; P< 0.001), respectively, indicating good model discrimination. Conclusions. This study concludes that APACHE II and OSF number measured prior to initiation of dialysis reliably predict outcomes of ARF patients requiring dialysis. The mortality rates increase as the APACHE II score or OSF number increases. For predicting mortality, the APACHE II score ≥ 24 was found to have 63% sensitivity and 96% specificity, and OSF number ≥ 2 had 81.6% sensitivity and 60.9% specificity.

Early detection of acute renal failure by serum cystatin C: A new opportunity for a hepatologist

Acute renal failure (ARF) is associated with high mortality. Presently, no specific therapy for ARF exists. Therefore, early detection of ARF is critical to prevent its progression. However, serum creatinine, the standard marker to detect ARF, demonstrates major limitations. We prospectively evaluated whether serum cystatin C detected ARF earlier than serum creatinine. In 85 patients at high risk to develop ARF, serum creatinine and cystatin C were determined daily. ARF was defined according to the Risk of renal dysfunction, Injury to the kidney, Failure of kidney function, Loss of kidney function, and ESRD (RIFLE) classification when creatinine increased by >/= 50% (R-criteria), by >/= 100% (I-criteria), or by >/= 200% (F-criteria). In analogy, ARF was detected when cystatin C increased by >/= 50%, by >/= 100%, or by >/= 200%. Forty-four patients developed ARF and 41 served as controls. In ARF by R-, I-, and F-criteria, the increase of cystatin C significantly preceded that of creatinine. Specifically, serum cystatin C increased already by >/= 50% 1.5 +/− 0.6 days earlier compared to creatinine. Serum cystatin C demonstrated a high diagnostic value to detect ARF as indicated by area under the curve of the ROC analysis of 0.82 and 0.97 on the two days before the R-criteria was fulfilled by creatinine. Cystatin C detected ARF according to the R-criteria with a sensitivity of 55% and 82% on these days, respectively. Cystatin C also performed excellently, detecting ARF defined by the I- and F-criteria two days prior to creatinine, and moderately well predicting renal replacement therapy in the further course of ARF. Additionally, low T(3)- or T(3)/T(4) syndrome, glucocorticoid deficiency and excess did not affect cystatin C levels, adding to its usefulness in critically ill patients with ARF. Serum cystatin C is a useful detection marker of ARF, and may detect ARF one to two days earlier than creatinine. (Kidney Int 2004;66:1115-1122)

Acute Renal Failure in Dogs After the Ingestion of Grapes or Raisins: A Retrospective Evaluation of 43 Dogs (1992–2002)

A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.

Insuffisances rénales aiguës médicamenteuses

Drug-induced acute renal failure (ARF) is common. Many therapeutic agents may induce ARF and there are numerous mechanisms that cause drug-induced ARF. The mechanisms may act at the vascular, glomerular or tubular levels. Drug toxicity may be related to the effects of the treatment itself or caused by hypovolaemia or disturbances of intrarenal haemodynamics. During the course of ARF, diagnosis should systematically include consideration of drug-related precipitating or predisposing factors. Drug-induced ARF is an undesirable iatrogenic occurrence that is largely avoidable and which has a more favourable prognosis than ARF of different pathogenesis. Treatment of this type of ARF is based on prevention. Any drug that is potentially toxic to the kidney should be prescribed in strict accordance with the indications and contraindications of the therapy. Prescription must take into account drug interactions and constitutional susceptibility (pre-exciting chronic renal failure, cirrhosis, old age). Dosage must be adapted to the glomerular filtration rate as estimated by the formula of Cockcroft-Gault. Hypovolaemia must be prevented or corrected.