Prevent Kidney Damage Research Articles

Beneficial effects montelukast, cysteinyl-leukotriene receptor antagonist, on renal damage after unilateral ureteral obstruction in rats.

Introductıon Ureteral obstruction is a common pathology and caused kidney fibrosis and dysfunction at late period. In this present, we investigated the antifibrotic and antiinflammatory effects of montelukast which is cysteinyl leukotriene receptor antagonist, on kidney damage after unilateral ureteral obstruction(UUO) in rats.Mateirıals and Methods 32 rats divided four groups. Group 1 was control, group 2 was sham, group 3 was rats with UUO and group 4 was rats with UUO which were given montelukast sodium (oral 10 mg/kg/day). After 14 days, rats were killed and their kidneys were taken and blood analysis was performed. Tubular necrosis, mononuclear cell infiltration and interstitial fibrosis scoring were determined histopathologically in a part of kidneys; nitric oxide(NO), malondialdehyde(MDA) and reduced glutathione(GSH) levels were determined in the other part of kidneys. Urea-creatinine levels were investigated at blood analysis. Statistical analyses were made by the Chi-square test and one-way analysis of variance (ANOVA).Results There was no difference significantly for urea-creatinine levels between groups. Pathologically, there was serious tubular necrosis and fibrosis in group 3 and there was significantly decreasing for tubular necrosis and fibrosis in group 4(p<0.005). Also, there was significantly increasing for NO and MDA levels; decreasing for GSH levels in group 3 compared the other groups(p<0.005).Conclusıon We can say that montelukast prevent kidney damage with antioxidant effect, independently of NO.

Protective effect of hydrogen sulfide on gentamicin-induced renal injury

Objective: We evaluated the potential protective effect of hydrogen sulfide (H2S) against GEN-induced nephrotoxicity in rats. Materials and methods: Twenty-four rats were randomly divided into four groups, each consisting of six animals as follows: (1) the rats were control, (2) intraperitoneally injected with GEN 14 consecutive days (100 mg/kg/day), (3) treated with GEN plus %0.9 saline intraperitoneally for 14 days and (4) treated with GEN plus sodium hydrogen sulfide (NaHS)-exogenous H2S donor (56 µmol/kg/day) for 14 days. After 15 days, rats were sacrificed and their kidneys were taken and blood analysis was performed. Twenty-four hours urine collections were obtained in standard metabolic cages a day before the rats were sacrificed. Tubular necrosis and interstitial fibrosis scoring were determined histopathologically in a part of kidneys; nitric oxide (NO), malondialdehyde (MDA) and reduced glutathione (GSH) levels were determined in the other part of kidneys. Statistical analyses were made by the chi-squared test and one-way analysis of variance. Results: Serum urea and creatinine levels were significantly higher in rats treated with GEN alone, than the rats in control and GEN + NaHS groups. The GSH levels in renal tissue of only GEN-treated rats were significantly lower than those in control group, and administration of NaHS to GEN-treated rats significantly increased the level of GSH. The group that was given GEN and NaHS had significantly lower MDA and NO levels in kidney cortex tissue than those that was given GEN alone. In rats treated with GEN + NaHS, despite the presence of mild tubular degeneration and tubular necrosis are less severe, and glomeruli maintained a better morphology when compared with GEN group. Discussion: We can say that H2S prevent kidney damage with antioxidant and anti-inflammatory effect.

Cardiorenal syndrome in acute heart failure: A vicious cycle?

Introduction and ObjectiveWorsening renal function has an unquestionably negative impact on prognosis in patients with acute heart failure (HF). In Portugal there is little information about the importance of this entity in HF patients admitted to hospital. The objective of this work was to assess the prevalence of cardiorenal syndrome and to identify its key predictors and consequences in patients admitted for acute HF. MethodsThis was a retrospective study of 155 patients admitted for acute HF. Cardiorenal syndrome was defined as an increase in serum creatinine of ≥26.5 μmol/l. Clinical, laboratory and echocardiographic parameters were analyzed and compared. Mortality was assessed at 30 and 90 days. ResultsCardiorenal syndrome occurred in 46 patients (29.7%), 5.4±4.4 days after admission; 66.7% (n=24) did not recover baseline creatinine levels. The factors associated with cardiorenal syndrome were older age, chronic renal failure, moderate to severe mitral regurgitation, higher admission blood urea nitrogen, creatinine and troponin I, and lower glomerular filtration rate. Patients who developed cardiorenal syndrome had longer hospital stay, were treated with higher daily doses of intravenous furosemide, and more often required inotropic support and renal replacement therapy. They had higher in‐hospital and 30‐day mortality, and multivariate analysis identified cardiorenal syndrome as an independent predictor of in‐hospital mortality. ConclusionsRenal dysfunction is common in acute HF patients, with a negative impact on prognosis, which highlights the importance of preventing kidney damage through the use of new therapeutic strategies and identification of novel biomarkers.

Síndrome cardiorrenal na insuficiência cardíaca aguda: um círculo vicioso?

Introduction and ObjectiveWorsening renal function has an unquestionably negative impact on prognosis in patients with acute heart failure (HF). In Portugal there is little information about the importance of this entity in HF patients admitted to hospital. The objective of this work was to assess the prevalence of cardiorenal syndrome and to identify its key predictors and consequences in patients admitted for acute HF. MethodsThis was a retrospective study of 155 patients admitted for acute HF. Cardiorenal syndrome was defined as an increase in serum creatinine of ≥26.5 μmol/l. Clinical, laboratory and echocardiographic parameters were analyzed and compared. Mortality was assessed at 30 and 90 days. ResultsCardiorenal syndrome occurred in 46 patients (29.7%), 5.4±4.4 days after admission; 66.7% (n=24) did not recover baseline creatinine levels. The factors associated with cardiorenal syndrome were older age, chronic renal failure, moderate to severe mitral regurgitation, higher admission blood urea nitrogen, creatinine and troponin I, and lower glomerular filtration rate. Patients who developed cardiorenal syndrome had longer hospital stay, were treated with higher daily doses of intravenous furosemide, and more often required inotropic support and renal replacement therapy. They had higher in‐hospital and 30‐day mortality, and multivariate analysis identified cardiorenal syndrome as an independent predictor of in‐hospital mortality. ConclusionsRenal dysfunction is common in acute HF patients, with a negative impact on prognosis, which highlights the importance of preventing kidney damage through the use of new therapeutic strategies and identification of novel biomarkers.

The role of uric acid in kidney fibrosis: experimental evidences for the causal relationship.

Hyperuricemia is a common finding in chronic kidney disease due to decreased uric acid clearance. The role of uric acid as a risk factor for chronic kidney disease has been largely debated, and recent studies suggested a role of uric acid in the causation and progression of kidney fibrosis, a final common pathway in chronic kidney disease. Uric acid and xanthine oxidase may contribute to kidney fibrosis mainly by inducing inflammation, endothelial dysfunction, oxidative stress, and activation of the renin-angiotensin system. Besides, hyperuricemia induces alterations in renal hemodynamics via afferent arteriolopathy and contributes to the onset and progression of kidney fibrosis. Xanthine oxidase inhibitors may prevent kidney damage via lowering uric acid and/or inhibiting xanthine oxidase. However, there is still no sufficient evidence from interventional clinical researches supporting the causal relationship between uric acid and kidney fibrosis. The effect and role of xanthine oxidase inhibitors in preventing kidney fibrosis and chronic kidney disease progression must be further explored by performing future large scale clinical trials.

Ultrasound treatment may help prevent kidney damage after surgery

Ultrasound treatment may help prevent kidney damage after surgery

Aegle marmelos Correa leaf extract prevents secondary complications in streptozotocin-induced diabetic rats and demonstration of limonene as a potent antiglycating agent

To study the antiglycating, antidiabetic and antioxidant properties of Aegle marmelos Correa leaf extract and identify the bioactive constituent. The effect of the chloroform extract of Aegle marmelos Correa was studied in streptozotocin-induced diabetic rats through evaluation of biochemical parameters. Antiglycation activity was assessed in vitro through measurement of total and specific advanced glycation end products, protein carbonyl formation and collagen solubility tests. Antioxidant potential was evaluated using the ferric-reducing antioxidant power assay and 2,2-diphenyl-1-picrylhydrazyl radical (DPPH) assays. Identification of the bioactive component was attempted through silica gel column chromatography and GC-MS analysis. In-vivo studies for 60 days revealed that the extract prevented kidney damage and other secondary complications. The chloroform extract at 16 μg could inhibit protein glycation by 44.33% and pentosidine formation by 59.31%, and could effectively inhibit protein carbonyl formation. It could scavenge DPPH radicals up to 85.26% (IC50: 26 μg). Bio-guided fractionation revealed limonene as the bioactive component, which could account for the antiglycating activity shown by the chloroform extract. The chloroform extract of Aegle marmelos demonstrated antidiabetic antiglycating and antioxidant activity, effectively preventing kidney damage and establishment of cataracts. Limonene is reported for the first time as possessing potent antiglycating activity and is non-toxic at the concentration used.

Attenuation of renal ischemia/reperfusion injury by a polysaccharide from the roots of Dipsacus asperoides

Renal ischemia–reperfusion (I/R) injury is a leading cause of acute renal failure and one of the major problems after I/R is the production of large amounts of reactive oxygen species (ROS). The present study was performed to evaluate the interference of a polysaccharide (WRDAP-1) from the roots of Dipsacus asperoides in I/R-induced renal injury in rats to determine whether it was mediated by the protective mechanism against oxidative stress to kidney. In vitro experiment, WRDAP-1 exhibited a potent scavenging ability on superoxide radical and hydroxyl radical. Renal protective effect of WRDAP-1 was evaluated in serum levels of blood urea nitrogen (BUN), creatinine, lactate dehydrogenase (LDH), superoxide dismutase (SOD) and serum malonaldehyde (MDA), as well as some renal tissue antioxidant enzymes activities like SOD glutathion peroxidase (GSH-Px) and catalase (CAT). Pretreatment with WRDAP-1 produced reduction in serum levels of BUN, creatinine and LDH caused by I/R injury and significantly improved serum enzymatic activity of SOD and serum MDA level. Additionally, antioxidant enzymes activities of SOD, GSH-Px and CAT in renal tissue were also elevated by WRDAP-1. Collectively, administration with WRDAP-1 significantly improved renal function of I/R rats especially in the rats treated with higher dose of the polysaccharide. Therefore the findings of this study imply that the protective effect of WRDAP-1 against renal I/R injury in rat kidneys could be due to its antioxidant and free radical scavenging activities. WRDAP-1 seems to be a highly promising agent for protecting tissues from oxidative damage and preventing kidney damage due to renal I/R.

The Reno-Protective Effects of Coconut Water on the Kidneys of Diabetic Wistar Rats

Diabetes Mellitus is one of the leading causes of end stage renal failure. In this present study the remedial effect of coconut water on alloxan-induced diabetes mellitus on the total body weight, kidney function and kidney cyto-architecture were studied. A total of eighteen (18) wistar rats were randomly divided into three experimental groups (n=6). Group I (Control) was fed on rat chow and water ad libitum and Group II and III were made diabetic by single intra peritoneal dose of 150mg/kg body weight of alloxan monohydrate. Group II were fed rat chow and water ad libitum and Group III fed a rat chow and coconut water ad libitum for 30 days. The result showed a statistical significant (P ˂ 0.05) reduction in weight, a significant increase in the renal function parameters (urea, creatinine, potassium, sodium and bicarbonate) due to diabetes and a significant reduction in these parameters following the administration of coconut water. The renal cyto-architecture also showed a protective/regenerative effect following treatment with coconut water. This finding may be beneficial in preventing kidney damage in diabetic patients.

Laboratory tests and intervention of early renal damage in children with Henoch-Schonlein purpura

Objective To investigate the efficacy of laboratory tests in the renal damage early diagnosis of children with Henoch-Schoalein purpura (HSP) and clinical effect of early intervention.Methods For the 143 HSP patients with normal repeated urine routine test findings,renal function biomarkers including urinary proteins ( immunoglobulin G (IgG),micro-albumin ( MA ),transferrin (TRF),a1 -microglobulin ( α1 -MG),β2-Microglobulin (β2-MG) ) and urinary enzymes ( N-acetyl-beta-D-glucosaminidase ( NAG ),γ-glutamyltransferase (y-GT) ) were detected to investigate the details of renal function changes.One hundred and thirty-one HSP patients,who had abnormal laboratory test findings of renal function biomarkers mentioned above,were randomly divided into control group ( n =65 ) and intervention group ( n =66 ),and both groups received comprehensive treatment including cimetidine,loratadine and calcium agents.However,66 patients in intervention group received low-dose heparin via micropump-based continuous intravenous infusion and regular oral diammonium glycyrrhizinate treatment.Sixty-five patients were enrolled in control group,without further treatment.Results Among the 143 patients with normal urine routine examination,131 cases (91.61％ ) had abnormal findings of renal function biomarkers.After therapy either for 2 months or 4 months,urine protein and urine enzymes were lower than before treatment,and the difference was significant (P ＜ 0.01 ).In the control group only β2-MG,NAG,γ-GT3 indexes significantly lowered at the end of 2 months ( P ＜0.01 ),and all parameters were significantly decreased at the end of 4 months ( P ＜0.01 ).Furthermore,Intervention group had lower levels of renal function biomarkers at the end of 2 months or 4 months,as compared with the control group,showing significant difference ( P ＜0.05 or P ＜0.01 ).Urinary IgG,MA,TRF,NAG recovered rapidly in the intervention group after 4 months and almost returned to the normal,but urinary α1-MG,β2-MG,γ-GT recovered slowly and still remained abnormal after 4 months due to the varying severity.After treatment for 4 months,the rate of urine testing abnormalities was higher in the control group than in the intervention group (36.92％ vs 6.10％ ),and the difference was significant (P ＜0.05).Conclusion Combined detection of renal function biomarkers is helpful for early diagnosis of renal damage in HSP patients.Early intervention with heparin and diammonium glycyrrhizinate can prevent kidney damage,delay disease progress.Early diagnosis and early intervention should be emphasized for the treatment strategy of the renal damage of children with HSP. Key words: Henoch-Schonlein purpura; Renal damage; Early diagnosis; Intervention; Children

Interest of microalbuminuria in preventing kidney damage during systemic lupus erythematosus (SLE) under corticoid therapy

This study aimed to evaluate the benefits of microalbuminuria in preventing kidney damage in systemic lupus erythemathosus. This was a prospective study of 6 months has focused on 25 patients of both sexes aged over 14 with SLE whose diagnosis was based on the criteria of the American College of Rheumatology, having a negative proteinuria at the dipstick (Ketodiastix(®)) and a balance sheet normal renal (creatinine and uraemia normal). Each month, samples of venous blood were achieved at the elbow in patients fasted for the night (12pm). The serum obtained was used for measurement of creatinine and urea, according to conventional methods, by a Hitachi 902(®) automated random type. The determination of urinary albumin by immuno-nephelometric method (Hitachi 902(®)), in search of microalbuminuria has involved the collection of urine over 24 hours in a sterile jar containing crystals of thymol as an antiseptic. In the presence of microalbuminuria, the dose of prednisone was progressively increased by 5 mg until no microalbuminuria. We found: 1) that creatinine and blood urea remained normal during the 6 months of study, 2) the disappearance of microalbuminuria first two months after increasing the daily dose of corticosteroid with a significant decrease of albuminuria from day 0 to day 180 (p = 0.001, day 180 vs day 0), 3) a female predominance with a sex ratio of 0.13. In conclusion, the regular dosage and systematic albuminuria to microalbuminuria appears to be a reliable means for diagnosis of lupus glomerulonephritis in the subclinical stage to prevent renal complications that occur during the Supported Lupus erythematosus.

Suppression of Nuclear Factor‐kappaB Activity Improves Renal Inflammation and Renal Morphology in Npr1 Gene‐disrupted Null Mutant Mice

Atrial and brain natriuretic peptides (ANP and BNP) play an important role in maintaining renal function and cardiovascular homeostasis via activating the membrane-bound guanylyl cyclase-A/natriuretic peptide receptor-A (GC-A/NPRA). The objective of the present study was to examine the consequences of Npr1 (coding for GC-A/NPRA) gene-disruption on renal inflammation, collagenesis, and remodeling in null mutant mouse model. In the present study, we utilized homozygous null mutant (Npr1−/−; 0-copy) and wild-type (Npr1+/+; 2-copy) mice. The histology results showed renal pathology characterized by increased matrix messangial expansion (MME) in 0-copy mice compared with 2-copy mice. An increased immunoexpression of macrophage/monocyte (ED1) was observed in the kidneys of 0-copy mice as compared with wild-type controls. Furthermore, a significant increased expression of pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α; 4-fold), interleukin-6 (IL-6; 4.5-fold), and transforming growth factor-β (TGF-β; 4-fold) were evident in 0-copy mice. Nuclear factor kappa-β (NF-kβ) binding and inhibitory kinase kB (IKKB) activity were increased significantly in the nuclear fractions in the kidneys of 0-copy mice as compared with wild-type mice. Treatment with NF-kβ antagonist, andrographolide, showed a marked attenuation in MME, renal fibrosis and ED1 immunoexpression in the kidneys of 0-copy mice. The present results indicate that Npr1 gene plays an important role in the prevention of kidney damage in the hypertensive disease state.

Assessing renal function - searching for the perfect marker continues!

Assessing renal function - searching for the perfect marker continues!

Prevention of diabetic nephropathy in Ins2+/−AkitaJ mice by the mitochondria-targeted therapy MitoQ

Mitochondrial production of ROS (reactive oxygen species) is thought to be associated with the cellular damage resulting from chronic exposure to high glucose in long-term diabetic patients. We hypothesized that a mitochondria-targeted antioxidant would prevent kidney damage in the Ins2+/−AkitaJ mouse model (Akita mice) of Type 1 diabetes. To test this we orally administered a mitochondria-targeted ubiquinone (MitoQ) over a 12-week period and assessed tubular and glomerular function. Fibrosis and pro-fibrotic signalling pathways were determined by immunohistochemical analysis, and mitochondria were isolated from the kidney for functional assessment. MitoQ treatment improved tubular and glomerular function in the Ins2+/−AkitaJ mice. MitoQ did not have a significant effect on plasma creatinine levels, but decreased urinary albumin levels to the same level as non-diabetic controls. Consistent with previous studies, renal mitochondrial function showed no significant change between any of the diabetic or wild-type groups. Importantly, interstitial fibrosis and glomerular damage were significantly reduced in the treated animals. The pro-fibrotic transcription factors phospho-Smad2/3 and β-catenin showed a nuclear accumulation in the Ins2+/−AkitaJ mice, which was prevented by MitoQ treatment. These results support the hypothesis that mitochondrially targeted therapies may be beneficial in the treatment of diabetic nephropathy. They also highlight a relatively unexplored aspect of mitochondrial ROS signalling in the control of fibrosis.

Basophils and the T helper 2 environment can promote the development of lupus nephritis

SummaryIn systemic lupus erythematosus (SLE) self-reactive antibodies can target the kidney (lupus nephritis) leading to functional failure and possible mortality. We report that activation of basophils by autoreactive IgE, causes their homing to lymph nodes, promoting TH2 cell differentiation, and enhancing the production of self-reactive antibodies that cause lupus-like nephritis in Lyn−/− mice. SLE patients also have elevated serum IgE, self-reactive IgE's, and activated basophils that express CD62L and the MHC Class II molecule, HLA-DR; parameters that were found to be associated with increased disease activity and active lupus nephritis. Basophils were also present in the lymph nodes and spleen of SLE patients. Thus, in Lyn−/− mice, basophils and IgE autoantibodies amplify autoantibody production that leads to lupus nephritis, and in SLE patients, the presence of IgE autoantibodies and activated basophils are factors associated with disease activity and nephritis.

Invited Commentary

Invited Commentary

Management of Sepsis-Induced Acute Kidney Injury

Acute kidney injury (AKI) occurs in a significant proportion of patients with severe sepsis, and is an important cause of mortality in such patients. Current concepts of pathogenesis of AKI are shifting from vasoconstriction-ischaemia induced injury to toxic and immune mediated injury and hyperaemic injury resulting in apoptosis of renal cells. Renal replacement therapy is the mainstay of management of AKI. Adequacy of dialysis is likely to be linked to better outcome, but there is still no clear consensus on the timing, modality, intensity or frequency of dialysis. Haemodynamically unstable patients usually require modes of continuous renal replacement therapy. Biocompatible dialyser membranes are likely to be safer than older cellulose membranes. Bicarbonate is preferred to acetate and lactate as dialysate buffer. Anticoagulation has to be undertaken with care to prevent excessive haemorrhage in the setting of already deranged haemostasis. Adequate volume resuscitation and maintenance of renal perfusion by the use of vasopressors is beneficial; norepinephrine is the vasopressor of choice. There is no place for the use of low- or renal-dose dopamine, mannitol or frusemide in the setting of sepsis-induced AKI, and in fact they may be detrimental. Prevention of kidney damage by nephrotoxic drugs and radio-contrast media is of vital importance. Careful dose management of nephrotoxic drugs will prevent renal injury. Hydration prior to administration of contrast media prevents nephrotoxicity, but the benefit of N-Acetylcysteine is unclear. Tight glycaemic control may have renoprotective effects, though its place in the management of severe sepsis is now controversial. No clear evidence of benefit is seen with other newer therapies.Keywords: Critical care; acute kidney injury; dialysis; renal replacementCitation: Rajapakse S, Rodrigo C, Wijewickrema ES. Management of Sepsis-Induced Acute Kidney Injury. Sri Lanka Journal of Critical Care 2009;1:3-14DOI: 10.4038/sljcc.v1i1.937

Does renal ageing affect survival?

The effects of ageing on progressive deterioration of renal function, both in human and experimental animals, are described elsewhere, but the effect of renal damage on overall survival and longevity is not yet clearly established. The wild-type animals of various genetic backgrounds, fed with regular diet, overtime develop severe age-associated nephropathy, that include but not limited to inflammatory cell infiltration, glomerulosclerosis, and tubulointerstitial fibrosis. Such renal damage significantly reduces their survival. Reducing renal damage, either by caloric restriction or by suppressing growth hormone (GH)/insulin-like growth factor-1 (IGF-1) activity could significantly enhance the longevity of these animals. Available survival studies using experimental animals clearly suggest that kidney pathology is one of the important non-neoplastic lesions that could affect overall survival, and that restoration of renal function by preventing kidney damage could significantly extend longevity. Careful long-term studies are needed to determine the human relevance of these experimental studies.

Antibiotics for acute pyelonephritis in children

AbstractBackgroundUrinary tract infection (UTI) is one of the most common bacterial infection in infants. The most severe form of UTI is acute pyelonephritis, which results in significant acute morbidity and may cause permanent renal damage. Published guidelines recommend treatment of acute pyelonephritis initially with intravenous (IV) therapy followed by oral therapy for seven to 14 days though there is no consensus on the duration of either IV or oral therapy.ObjectivesTo determine the benefits and harms of different antibiotic regimens for the treatment of acute pyelonephritis in children.Search strategyWe searched the Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, reference lists of articles and abstracts from conference proceedings without language restriction.Date of most recent search: June 2004.Selection criteriaRandomised and quasi‐randomised controlled trials comparing different antibiotic agents, routes, frequencies or durations of therapy in children aged 0 to 18 years with proven UTI and acute pyelonephritis were selected.Data collection and analysisTwo reviewers independently assessed trial quality and extracted data. Statistical analyses were performed using the random effects model and the results expressed as relative risk (RR) for dichotomous outcomes or weight mean difference (WMD) for continuous data with 95% confidence intervals (CI).Main resultsEighteen trials (2612 children) were eligible for inclusion. No significant differences were found in persistent renal damage at six months (one trial, 306 infants: RR 1.45, 95% CI 0.69 to 3.03) or in duration of fever (WMD 0.80, 95% CI ‐4.41 to ‐ 6.01) between oral cefixime therapy (14 days) and IV therapy (three days) followed by oral therapy (10 days). Similarly no significant differences in persistent renal damage (three trials, 315 children: RR 0.99, 95% CI 0.72 to 1.37) were found between IV therapy (3‐4 days) followed by oral therapy and IV therapy for 7‐14 days. In addition no significant differences in efficacy were found between daily and thrice daily administration of aminoglycosides (one trial, 179 children, persistent symptoms at three days: RR 1.98, 95% CI 0.37 to 10.53).Authors' conclusionsThese results suggest that children with acute pyelonephritis can be treated effectively with oral cefixime or with short courses (2‐4 days) of IV therapy followed by oral therapy. If IV therapy is chosen, single daily dosing with aminoglycosides is safe and effective. Trials are required to determine the optimal total duration of therapy and if other oral antibiotics can be used in the initial treatment of acute pyelonephritis.Plain language summaryOral antibiotics may be as effective as the combination of injection and oral antibiotics for kidney infections in childrenAcute pyelonephritis refers to infection of the kidneys and is the most severe form of urinary tract infection (UTI). It causes high fever, vomiting, stomach pain, irritability and poor feeding in infants. Usual treatment is antibiotics given first by injection (IV) and then orally for 7‐14 days to clear the infection and prevent kidney damage. These results suggest that children with acute pyelonephritis can be treated effectively with oral cefixime or with short courses (2‐4 days) of IV therapy followed by oral therapy. If IV therapy is chosen, single daily dosing with aminoglycosides is safe and effective. Copyright © 2006 The Cochrane Collaboration. Published by John Wiley &amp; Sons, Ltd.

TREATMENT OF NEUROGENIC DETRUSOR OVERACTIVITY IN SPINAL CORD INJURED PATIENTS BY CONDITIONAL ELECTRICAL STIMULATION

The feasibility of automatic event driven electrical stimulation of the dorsal penile/clitoral nerve in the treatment of neurogenic detrusor overactivity (NDO) was evaluated in individuals with spinal cord injury. The study included 2 women and 14 men older than 18 years with NDO, bladder capacity below 500 ml and complete or incomplete suprasacral spinal cord injury. Detrusor pressure (Pdet) was recorded during ordinary, natural bladder filling. In a similar subsequent recording Pdet was used to trigger electrical stimulation when pressure exceeded 10 cm H2O. Of the 16 patients enrolled in this study 13 had increased bladder capacity together with a storage pressure decrease as a result of automatic, event driven electrical stimulation. In 2 patients stimulation could not inhibit the first undesired contraction, leakage occurred and finally 1 could not tolerate stimulation. During stimulated filling Pdet never exceeded 55 cm H2O. Thus, storage pressure was sufficiently low to prevent kidney damage. An average bladder capacity increase of 53% was achieved. This study demonstrates the feasibility of automatic, event driven electrical stimulation in the treatment of NDO. Although the setup in this experiment is not suitable in a clinical setting, the treatment modality is promising and it warrants further investigation.