Browsing by Author "S.S. Rathore"

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Acute kidney injury in patients with human immunodeficiency virus infection
(Wolters Kluwer Medknow Publications, 2015) J. Prakash; T. Gupta; S. Prakash; S.S. Rathore; Usha; S. Sunder
Acute kidney injury (AKI) is an important cause of hospitalization and morbidity in human immunodeficiency virus (HIV)-positive patients. However, the data on AKI in such patients is limited. The aim of the present study was to analyze the incidence, causes and outcome of AKI in HIV-positive patients from our antiretroviral therapy centre. All HIV-positive patients were evaluated for evidence of clinical AKI. AKI was noted in 138/3540 (3.9%) patients. Of 138 AKI patients, 96 (69.6%) had acquired immuno deficiency syndrome and 42 (30.4%) were HIV seropositive. Majority of AKI patients belonged to AKI network (AKIN) Stage II (42%) or III (48.5%) at presentation. Prerenal, intrinsic and postrenal AKI were noted in 53.6%, 44.2% and 2.2% of cases, respectively. Hypovolemia (44.2%) and sepsis (14.5%) contributed to AKI in vast majority of cases. AKI was multifactorial (volume depletion, sepsis and drugs) in 39% of patients. Acute tubular necrosis (ATN) was the most common intrinsic lesion. Acute interstitial nephritis and diffuse endocapillary proliferative glomerulonephritis were noted in five and two cases, respectively. In-hospital mortality was 24.64%. Lower CD4 count, decreased serum albumin level and Stage 4 WHO disease were associated with higher mortality. At 3 months or more follow-up complete recovery of renal function, chronic kidney disease Stage 3-5 and progression to end stage renal disease were noted in 58.69%, 14.5% and 2.2% of cases, respectively. Thus, prerenal factors and ischemic ATN were the most common cause of AKI in HIV-infected patients. Recovery of renal function was seen in 59% of cases, but AKI had high in-hospital mortality.
Causes of death in renal transplant recipients with functioning allograft
(2012) B. Ghosh; J. Prakash; S.S. Rathore; S. Singh; A. Soni
The survival of transplant recipients is significantly lower than age-matched controls in the general population. The aim of this study was to analyze the trends in mortality of renal allograft recipients at our centre. We retrospectively analyzed data from all patients who were transplanted between October 1988 and June 2010 and were followed at our center. Patients were considered to have death with graft function (DWGF) if death was not preceded by return to dialysis or re-transplantation. The study included 98 renal allograft recipients (male : female - 7.99 : 1). The mean recipient and donor ages were 35.06 11.84 (range: 15-69) and 41.17 10.44 (range: 22-60) years, respectively. Basic kidney diseases were CGN (chronic glomerulonephritis) (60.20%), CIN (chronic interstitial nephritis) (15.31%), DN (diabetic nephropathy) (8.16%), ADPKD (autosomal dominant polycystic kidney disease) (2.04%) and others (14.29%). They were followed up for a mean 79.91 60.05 patient-months. Mortality occurred in 25 (25.51%) patients (male : female - 4 : 1). Causes of death were sepsis/infection (36%), coronary artery disease (28%), CVA (8%), failed graft (4%), and rest unknown (24%). DWGF was 88% of total death and contributed to 78.57% of total graft loss. Overall patient survival at 1, 5, 10, and 15 years were 90.8%, 80.2%, 65.6%, and 59.1%, respectively (Kaplan-Meier analysis). Those who died exhibited significant differences in recipient's age (median 40 years vs 31 years, P=0.007), pretransplantation hypertension (HTN) (100% vs 65.75%, P>0.001), post-transplant infection (76% vs 42.47%, P=0.005), coronary artery disease (28% vs 1.37%, P>0.001), and serum creatinine at last follow up (median 2.3mg/dL vs 1.56mg/dL, P=0.003). Cardiovascular disease, in addition to infection, is an important cause of death during the first 15 years following renal transplantation even in nondiabetic recipients. Death with functioning graft is of concern.
Hospital-acquired acute kidney injury in medical, surgical, and intensive care unit: A comparative study
(2013) T.B. Singh; S.S. Rathore; T.A. Choudhury; V.K. Shukla; D.K. Singh; J. Prakash
Acute kidney injury (AKI) is a common complication in hospitalized patients. There are few comparative studies on hospital-acquired AKI (HAAKI) in medical, surgical, and ICU patients. This study was conducted to compare the epidemiological characteristics, clinical profiles, and outcomes of HAAKI among these three units. All adult patients (>18 years) of either gender who developed AKI based on RIFLE criteria (using serum creatinine), 48 h after hospitalization were included in the study. Patients of acute on chronic renal failure and AKI in pregnancy were excluded. Incidence of HAAKI in medical, surgical, and ICU wards were 0.54%, 0.72%, and 2.2% respectively (P < 0.0001). There was no difference in age distribution among the groups, but onset of HAAKI was earliest in the medical ward (P = 0.001). RIFLE-R was the most common AKI in medical (39.2%) and ICU (50%) wards but in the surgical ward, it was RIFLE-F that was most common (52.6%). Acute tubular necrosis was more common in ICU (P = 0.043). Most common etiology of HAAKI in medical unit was drug induced (39.2%), whereas in surgical and ICU, it was sepsis (34% and 35.2% respectively). Mortality in ICU, surgical and medical units were 73.5%, 43.42%, and 37.2%, respectively (P = 0.003). Length of hospital stay in surgical, ICU and medical units were different (P = 0.007). This study highlights that the characters of HAAKI are different in some aspects among different hospital settings. © 2013 Indian Journal of Nephrology.
Urinary MCP-1 as diagnostic and prognostic marker in patients with lupus nephritis flare.
(2012) R.G. Singh; Usha; S.S. Rathore; S.K. Behura; N.K. Singh
This study aimed to assess correlation of urinary monocytic chemoattractant protein-1 (UMCP-1) with severity of lupus nephritis and its role as predictor of outcome. Twenty patients with lupus nephritis flare were included in the study. Ten patients in each group of stable systemic lupus erythematosus and non-renal flare were taken as controls. Biopsy was done to define lupus nephritis stage. UMCP-1 levels were measured in all patients at the time of entry and at four and eight weeks of follow-up. Mild, moderate and severe lupus nephritis flare was noted in one, five and 15 patients, respectively. UMCP-1 levels were high in patients with severe lupus nephritis flare (2.74 ± 0.95 ng/mg creatinine) as compared to patients with moderate (1.43 ± 0.46 ng/mg creatinine) and mild lupus nephritis flare (0.76 ± 0.57 ng/mg creatinine) (P = 0.0093). Baseline mean UMCP-1 levels in lupus nephritis flare, non-renal flare and stable SLE patients were 2.32 ± 1.06, 0.171 ± 0.03 and 0.213 ± 0.026 ng/mg creatinine, respectively. The difference among the three groups was very significant (P < 0.001). Also, mean UMCP-1 levels correlated significantly with severity of lupus nephritis class (P = 0.0358). During follow-up, 15 patients achieved complete or partial remission, and in these patients mean UMCP-1 levels had significant decline at eight weeks (P < 0.0001). However, mean UMCP-1 levels in the remaining five non-responders did not show significant changes at four and eight weeks (P = 0.4858). Mean UMCP-1 levels were significantly higher in the lupus nephritis flare group as compared to non-renal flare and stable patients. Baseline mean UMCP-1 levels significantly correlated with both lupus nephritis class and severity of lupus nephritis flare, hence UMCP-1 could be used as a non-invasive marker for the judgement of lupus flare and lupus nephritis class.