scholarly journals NEPHROTOXICITY ATTRIBUTED TO MEGLUMINE ANTIMONIATE (GLUCANTIME) IN THE TREATMENT OF GENERALIZED CUTANEOUS LEISHMANIASIS

1999 ◽  
Vol 41 (1) ◽  
pp. 33-37 ◽  
Author(s):  
M.L.O. RODRIGUES ◽  
R.S. COSTA ◽  
C.S. SOUZA ◽  
N.T. FOSS ◽  
A.M.F. ROSELINO
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Side Effects ◽  
Serum Creatinine ◽  
Cutaneous Leishmaniasis ◽  
Urine Osmolarity ◽  
Hepatic Enzyme ◽  
Meglumine Antimoniate ◽  
Tubular Necrosis ◽  
Electrocardiographic Abnormalities

Background: Pentavalent antimonials have became of basic importance for the treatment of leishmaniasis. Their most severe side effects have been reported to be increased hepatic enzyme levels and electrocardiographic abnormalities. Nephrotoxicity has been rarely related. Observations: We report a case of generalized cutaneous leishmaniasis involving a 50-year old male patient who was submitted to treatment with meglumine antimoniate (Glucantime). He developed acute renal failure (ARF) due to acute tubular necrosis (ATN), followed by death after receiving a total of 53 ampoules of Glucantime. Conclusions: The treatment with Glucantime was responsible by ARF diagnosed in this patient. The previous urine osmolarity and serum creatinine levels were normal and the autopsy showed ATN. It should be pointed out if ARF may also be explained by massive deposits of immunocomplexes by leishmania antibodies and antigens due to the antigenic break by the antimonial compound, since our patient presented countless lesions covering the entire tegument, similar to the Hexheimer phenomenon, but at the autopsy no glomerular alterations were seen.

scholarly journals P. falciparum Malaria induced Renal impairment

2019 ◽  
Vol 5 (6) ◽  
pp. 220-223
Author(s):  
Tarkeswar Aich ◽  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Dysfunction ◽  
Falciparum Malaria ◽  
Acute Tubular Necrosis ◽  
Mean Value ◽  
Intravascular Haemolysis ◽  
Tubular Necrosis ◽  
Oliguric Renal Failure

Introduction: The involvement of the kidney in falciparum malaria has been known for decades. In 1944, Spitz observed acute renal failure due to falciparum infection in soldiers during World War II. This observation was later supported by other workers who detected oliguria developing in patients with black water fever. The initial clinical pattern is that of reversible renal dysfunction or pre-renal azotemia, which rapidly progresses to acute tubular necrosis if treatment is not started early. Patients with malaria induced renal failure are hypercatabolic with blood urea and serum creatinine levels rising rapidly.Oliguric as well non-oliguric renal failure are observed and duration of oliguric renal failure ranges from a few days to several weeks depending on the severity of renal dysfunction. Acute renal failure in falciparum malaria is usually associated either with acute intravascular haemolysis or heavy parasitemia. Acute renal failure in falciparum malaria is also observed in patients with severe intravascular haemolysis resulting in haemoglobinuria. It may be induced by malarial fever or by anti-malarial drugs in a patient with or without G6-PD deficiency. Materials and Methods: This is a hospital based cross sectional study carried out in a total of 50 cases of acute renal failure who were selected from diagnosed patients of P. falciparum malaria. Cases were confirmed either by P. falciparum antigen test and/or peripheral blood smear test(both thick and thin smear).Malarial ARF (MARF) is diagnosed when serum creatinine level > 3 mg/dl, and/or urine output < 400 ml/24hrs despite adequate rehydration. Result: Out of 174 cases of falciparum malaria 50 patients (28.7%) had acute renal failure in falciparum malaria. 36 (72%) cases were males and 14 (28%) were females, indicating a much higher incidence in males. Approximately 78% of the cases in the present study were below the age of 40 years. The youngest was 15 years old and the oldest was 61 years old (Mean age – 32 ± 11.6 years). All were febrile (100%) and a majority had oliguria or anuria (72%); jaundice was detected in 30 (60%) patients on presentation. Hepatomegaly & Splenomegaly were found in 76% & 66% of the cases respectively. Out of the total 50 cases of malaria induced ARF, 14 cases (28%) had pre-renal ARF while in the majority, 72% the clinical course was that of ATN. The pathogenesis of ATN in the 36 cases was found to be heavy parasitaemia in 40% of the cases, IV hemolysis with haemoglobinuria in 3 (6%) of cases; and cholestatic jaundice in 26% of falciparum patients. Examination of the urinary sediments revealed that albumin was present in urine in 40 cases (80%). Majority of the patients had significant rise in blood urea level with a mean value of 177 mg. S. creatinine levels ranged between 3.2 - 13.6 mg with a mean value of 7.83 mg. The mean creatinine clearance rate was 11.71 ml/min. The overall mortality rate was 26%. Conclusion: AKI is common in Falciparum malaria. The pathogenesis of AKI is largely unknown but may be related to the erythrocyte sequestration and agglutination within the renal microcirculation interfering with flow and metabolism. Clinically and pathologically, this syndrome manifests as Pre-renal azotemia and acute tubular necrosis. Acute renal failure may occur simultaneously with other vital-organ dysfunction (in which case the mortality risk is high) or may progress as other disease manifestations resolve. Early dialysis or hemofiltration considerably enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure. Severity of oliguria and presence of one or more associated complications like pulmonary oedema, acidosis, and altered sensorium have considerable influence on the outcome of the patients.

Relationship Between Level of Heart Type Fatty Acid Binding Protein (Before and after Procedures) with Acute Renal Failure after PCI in Patients Under PCI

2020 ◽  
Vol 20 (1) ◽  
pp. 41-46
Author(s):  
Habib Haybar ◽  
Ahmad R. Assareh ◽  
Mina Mohammadzadeh ◽  
Shahla A. Hovyzian
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Fatty Acid Binding Protein ◽  
Coronary Intervention ◽  
Good Test ◽  
Fatty Acid Binding ◽  
Percutaneous Coronary ◽  
Before And After ◽  
Specific Factors

Background & Objective: Acute renal failure (AKI) is one of the most important complications of PCI. Due to delay in creatinine increase, we need specific factors to detect AKI earlier. The aim of this study is to evaluate the valuable factors by focusing on HFAB-P that can be predictive for AKI after Percutaneous Coronary Intervention (PCI). Methods: This prospective study was performed on 95 patients (55 males and 44 females aged between 49-78 years) under PCI in Golestan and Imam Khomeini hospitals in Ahvaz. Patients were divided into three groups based on the development of AKI after the procedure: no AKI, severe AKI (doubling of serum creatinine or needing dialysis) and any type of AKI (increased creatinine ≥ 0/3 mg/dl or a 50% increase in the means of 1/5 times serum creatinine). The demographic and clinical characteristics of the patients, the medical history and the results of the HFABP marker, GFR, and creatinine before and after PCI were evaluated for all patients. Results: The progenies showed 6 patients with severe AKI, 17 patients with any type of AKI, and 72 patients without AKI. Diabetes (P = 0.003), hypertension (P = 0.027), gender of patients (P = 0.025) and hospital admission days (P <0.001) were significantly different among the groups. Patients' age and positive troponin were significantly higher in patients with AKI. HFABP was the only factor that had significant changes before and after PCI (P <0.001). The cut-off value of HFABP was 4.69 with 95.6% sensitivity and 84.7% specificity. It has a good negative predictive value of 98.39% which suggests it to be a good test for the AKI prediction. Glomerular Filtration Rate (GFR) and creatinine (Cr) were significantly different after PCI (P <0.001). Conclusion: HFABP can be considered as a predictor for AKI after PCI. Moreover, our study suggests that evaluating several parameters such as Cr and GFR before and after PCI can predict the AKI development after PCI.

Acute Renal Failure Caused by Imiquimod 5% Cream in a Renal Transplant Patient: Review of the Literature on Side Effects of Imiquimod

Dermatology ◽  
2011 ◽  
Vol 222 (2) ◽  
pp. 109-112 ◽  
Author(s):  
J. Santos-Juanes ◽  
A. Esteve ◽  
A. Mas-Vidal ◽  
P. Coto-Segura ◽  
E. Salgueiro ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Side Effects ◽  
Renal Transplant ◽  
Renal Transplant Patient ◽  
Transplant Patient ◽  
Review Of The Literature

Frequency of factors leading to acute renal failure in obstetric patients.

2021 ◽  
Vol 28 (05) ◽  
pp. 640-646
Author(s):  
Shaheena Zafar ◽  
Riffat Jaleeel ◽  
Kouser Karim Lodhani
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Placental Abruption ◽  
Post Partum ◽  
Common Factor ◽  
Tertiary Care ◽  
Cross Sectional Study ◽  
Care Hospital ◽  
Cross Sectional

Objective: To determine the frequency of factors leading to acute renal failure in obstetric patients. Study Design: Cross Sectional study. Setting: Department of Obstetrics and Gynecology, Civil Hospital Karachi, Tertiary Care Hospital. Period: July 2015- Jan 2016. Material & Methods: Total 250 women during pregnancy and within 42 days after delivery who were diagnosed as ARF were included. Serum creatinine was done on admission and then after 24 hours of delievery. Those with urine output < 30ml / hour and serum creatinine > 1.5 mg / dl were recruited. All data was recorded on proforma. Results: The average age of the women was 29.36±5.87 years. Post-partum hemorrhage was the important and common factor i.e. 40.4%, followed by placental abruption 25.6%, Severe pre-eclampsia 18.4%, puerperal sepsis 8.4% and eclampsia 7.2%. Conclusion: Ante partum hemorrhage like placental abruption, eclampsia and preeclampsia, and postpartum hemorrhages’ are the major causes of obstetrical ARF. Good antenatal care and provision of universal health facility can prevent this dangerous condition. Though it is a treatable and curable complication, but if not diagnosed and treated timely, it can lead to significant maternal morbidity and mortality.

scholarly journals Comparison of Oral Zinc Sulfate with Systemic Meglumine Antimoniate in the Treatment of Cutaneous Leishmaniasis

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Mohamad Javad Yazdanpanah ◽  
Mahnaz Banihashemi ◽  
Fakhrozaman Pezeshkpoor ◽  
Mohammad Khajedaluee ◽  
Sororozaman Famili ◽  
...  
Keyword(s):  
Side Effects ◽  
Cutaneous Leishmaniasis ◽  
Side Effect ◽  
Zinc Sulfate ◽  
Cure Rate ◽  
Meglumine Antimoniate ◽  
Treatment Groups ◽  
Significant Difference

The purpose of this study was to investigate comparison between oral zinc sulfate and meglumine antimoniate in the treatment of cutaneous leishmaniasis (CL). So 100 patients with CL were included and randomly divided into two groups. The first group was treated with oral zinc sulfate (10 mg/kg/day during 45 days period), and the second group was treated with systemic meglumine antimoniate (20 mg/kg/day intramuscularly for 20 days). Acceptable cure after completing 45 days of followup occurred in 30.2% of lesions in first group, while this was 35.5% for the second group. There is not any significant difference between the two treatment groups (P=0.42). Serious side effects resulting in treatment discounting occurred in only meglumine antimoniate group. Although cure rate of systemic meglumine antimoniate group was better the treatment with zinc sulfate is much easier, cheaper, more convenient in consumption, safer, and nearly close cure percentage to systemic meglumine antimoniate injections without serious side effect.

scholarly journals Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil

2005 ◽  
Vol 47 (6) ◽  
pp. 315-320 ◽  
Author(s):  
Elizabeth De Francesco Daher ◽  
Geraldo Bezerra da Silva Júnior ◽  
Marúsia Thomaz Ferreira ◽  
Fernando Antonio de Sousa Barros ◽  
Tiago Magalhães Gurgel ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Involvement ◽  
Clinical Manifestations ◽  
Signs And Symptoms ◽  
Hemodynamic Instability ◽  
Human Rabies ◽  
Tubular Necrosis ◽  
Post Mortem Findings ◽  
Histopathologic Findings

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 ± 34 days). The time until death ranged from one to nine days (mean 3.3 ± 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.

scholarly journals Incidence of Acute Renal Failure in Full Term Neonates with Birth Asphyxia

2019 ◽  
Vol 4 (1) ◽  
pp. 671-674
Author(s):  
Chandra Bhushan Jha ◽  
Akhil Tamrakar
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Renal Injury ◽  
Urine Output ◽  
Birth Asphyxia ◽  
Full Term ◽  
Acute Renal Injury ◽  
Term Neonates ◽  
Oliguric Renal Failure

Introduction: Birth asphyxia is an eventuality having far reaching consequences in the neonatal period. Hypoxia and ischemia can cause damage to almost every tissue and organ in the body and various target organs involved. Renal insult is a recognized complication of birth asphyxia and carries a poor prognosis. Timely detection of renal dysfunction and appropriate management may favorably alter the prognosis in many neonates with birth asphyxia. Objective: The present study was done to find out the incidence of acute renal failure in the full term neonates with birth asphyxia. Methodology: A cross sectional study was conducted at Birat Medical College Teaching Hospital, Morang, Nepal from 1st September 2017 to 28th February 2018. Fifty full term neonates born with Apgar score of <6 at 5 minutes and fulfilling inclusion criteria were enrolled in the study. Asphyxiated neonates having Serum creatinine >1.5gm/dl or urine output<1ml/kg/hr were labeled as cases of Acute Renal Failure. Blood sample for serum creatinine was collected at 24hrs, 48 hrs and 72 hrs of life. Results A total of 50 term asphyxiated neonates were enrolled in the present study. Among them 54% and 46% were males and females respectively with male to female ratio of 1.2:1. In the present study 62% of cases developed acute renal failure in either of the first three days of life with mean urine output 1.02±0.27ml/kg/hr and mean serum creatinine of 1.49±0.32 mg/dL. The incidence of oliguric renal failure was 52% and non oliguric renal failure was 48%.The association between serum creatinine and urine output was statistically significant. Conclusion: In the present study birth asphyxia has been an important cause of neonatal acute renal injury, revealing 31 (62%) cases. Monitoring urine output and serum creatinine has helped in detecting the asphyxiated neonates with acute renal injury in the early stage.

scholarly journals An evaluation of antioxidant effects on recovery from postischemic acute renal failure.

1994 ◽  
Vol 4 (8) ◽  
pp. 1588-1597
Author(s):  
R A Zager ◽  
S M Fuerstenberg ◽  
P H Baehr ◽  
D Myerson ◽  
B Torok-Storb
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Dna Fragmentation ◽  
Proliferating Cell Nuclear Antigen ◽  
Antigen Expression ◽  
Nuclear Antigen ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tubular Necrosis ◽  
Proliferating Cell

Xanthine oxidase (XO) activity and hydroxyl radical (.OH) formation are widely proposed mediators of renal reperfusion injury, potentially altering the severity of, and recovery from, postischemic acute renal failure. The goal of this study was to ascertain whether combination XO inhibitor (oxypurinol) and .OH scavenger (Na benzoate) therapy, given at the time of renal ischemia, alters the extent of: (1) tubular necrosis and filtration failure; (2) DNA fragmentation/apoptosis (assessed in situ by terminal deoxynucleotidyl transferase reactivity); (3) early tubular regenerative responses (proliferating cell nuclear antigen expression; (3H)thymidine incorporation); and (4) the rate and/or degree of functional and morphologic repair. The effects of XO inhibition, .OH scavengers, and "catalytic" iron (FeSO4) on human proximal tubular cell proliferation in vitro were also assessed with a newly established cell line (HK-2). Male Sprague-Dawley rats were subjected to 35 min of bilateral renal arterial occlusion with or without oxypurinol/benzoate therapy. These agents did not alter the extent of tubular necrosis or filtration failure, proliferating cell nuclear antigen expression or thymidine incorporation, or the rate/extent of renal functional/morphologic repair. DNA fragmentation did not precede tubular necrosis, and it was unaffected by antioxidant therapy. By 5 days postischemia, both treatment groups demonstrated regenerating epithelial fronds that protruded into the lumina. These structures contained terminal deoxynucleotidyl transferase-reactive, but morphologically intact, cells, suggesting the presence of apoptosis. Oxypurinol and .OH scavengers (benzoate; dimethylthiourea) suppressed in vitro tubular cell proliferation; conversely, catalytic Fe had a growth-stimulatory effect. These results suggest that: (1) XO inhibition/.OH scavenger therapy has no discernible net effect on postischemic acute renal failure; (2) DNA fragmentation does not precede tubular necrosis, suggesting that it is not a primary mediator of ischemic cell death; and (3) antioxidants can be antiproliferative for human tubular cells, possibly mitigating their potential beneficial effects.

scholarly journals Acute Renal Failure in a Tertiary Care Center in Nepal

2005 ◽  
Vol 44 (158) ◽  
Author(s):  
Sudha Khakurel ◽  
P R Satyal ◽  
R K Agrawal ◽  
P K Chhetri ◽  
R Hada
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Bacillary Dysentery ◽  
Care Center ◽  
Tertiary Care ◽  
Acute Interstitial Nephritis ◽  
Female Age ◽  
Tubular Necrosis ◽  
Common Causes ◽  
Urate Nephropathy

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Outof which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35years and 9 cases were below 10 years.Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstreticalcomplications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases.Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemicsyndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl,mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis,fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration ofhospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, tenexpired, two recovered partially, two progressed to chronic renal failure and two left against medical advice.Overall mortality was 22.2%.Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS wasexclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause ofacute renal failure in our country.

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