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.
BackgroundThe epidemiology of acute kidney injury (AKI) differs from country to country and varies from center to center within a country. Owing to the absence of a central registry, data on overall epidemiology of AKI are scanty from India.MethodsThis study aimed at describing changes in epidemiology of community-acquired AKI (CAAKI) over a time span of 26 years in two study periods, namely, 1983–95 and 1996–2008.ResultsWe studied 2405 (1375 male and 1030 female) cases of AKI in the age range 1–95 (mean: 40.32) years. The incidence of CAAKI in 1983–95 and 1996–2008 was 1.95 and 4.14 per 1000 admission, respectively (P < 0.01). Obstetrical AKI has decreased because of the declining number of post-abortal AKI. Surgical AKI decreased from 13.8% in 1983–95 to 9.17% in 1996–2008(P < 0.01). Malarial AKI increased significantly from 4.7% in the first half of the study to 17% in the later period (P < 0.01). Diarrhea-associated AKI had significantly decreased from 36.83% in 1983–95 to 19% in 1996–2008 (P < 0.01). Sepsis-related AKI had increased from 1.57% in 1983–95 to 11.43% in 1996–2008 (P < 0.01). Nephrotoxic AKI showed an increasing trend in recent years (P < 0.01) and mainly caused by rifampicin and NSAIDs. Liver disease-related AKI increased from 1.73% in 1983–95 to 3.17% in 1996–2008 (P < 0.01). Myeloma-associated acute renal failure (ARF) accounted for 1.25% of the total number of ARF cases in the period 1996–2008. HIV infection contributed to 1.65% of ARF of the total number of AKI cases in the second period (1996–2008). Incidence of renal cortical necrosis (RCN) decreased significantly from 5.8% in 1983–95 to 1.3% in 1996–2008 of the total number of ARF cases (P < 0.01). However, during the same period ARF due to acute tubular necrosis, acute glomerulonephritis and acute interstitial nephritis remained unchanged. The mortality rate from AKI decreased significantly from 20% in 1983–95 to 10.98% in 1996–2008 (P < 0.01).ConclusionsThe epidemiological characteristics of CAAKI have changed over the past three decades. There has been an increase in the overall incidence of ARF with the changing etiology of AKI in recent years. Incidences of obstetrical, surgical and diarrheal AKI have decreased significantly, whereas those of AKI associated with malaria, sepsis, nephrotoxic drugs and liver disease have increased. RCN has decreased significantly. In contrast to developed nations, community-acquired AKI is more common in developing countries. It often affects younger individuals and is caused by single and preventable diseases.
Recent data regarding the clinical and histopathologic spectrum of crescentic glomerulonephritis (CSGN) among the Indian adult population is unknown. Our aim is to study the clinicopathological features and outcome of CSGN. It is a retrospective observational study from a tertiary care hospital in India over 3.5 years. Biopsy-proven cases of CSGN (i.e., >50% crescents in glomeruli) were included in the study. Cases with insufficient data were excluded. There were 34 cases of CSGN, accounting for an incidence of 5.5% among kidney biopsies. The mean age was 32.2 ± 16.09 years, with male to female ratio of 12:22. Clinical presentations of CSGN include rapidly progressive glomerulonephritis in 23 (67.7%), chronic renal failure (CRF) in seven (20.5%), nephrotic syndrome in two (5.8%) and acute nephritic syndrome in two (5.8%) patients. The immunological profile of CSGN showed MPO-ANCA in nine (26.4%), PR3-ANCA in one (2.9%), both PR3 and MPO-ANCA in one (2.9%), anti-GBM antibody in five (14.7%) and lupus nephritis in six (17.6%) patients. All the three antibodies were present in one patient. The percentage of glomeruli showing crescents were 100% in nine (26.4%) and ≥80% in seven (20.5%) patients. Type of crescents seen were cellular in 11 (32.3%) and fibrocellular in 22 (64.7%) patients and fibrous in one (2.9%) patient. Interstitial fibrosis was found in seven (20.5%) patients. Dialysis dependency was seen in 11 (32.3%) patients. After 3 months of follow-up, mortality was seen in three (8.8%), remission in eight (23.5%), CRF in 15 (44.1%) and ESRD in five (14.7%) patients. CSGN carries a poor prognosis. The disorder may have an insidious onset and a slowly progressive course. ANCA, anti-GBM-antibody and anti-dsDNA can coexist in CSGN.
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.
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.
Background: Renal amyloidosis is a major cause of morbidity and mortality among the patients of systemic amyloidosis.
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