The incidence of acute kidney injury in pregnancy (P-AKI) has declined significantly over the last three decades in developing countries. However, it is still associated with significant fetomaternal mortality and morbidity. The diagnosis of P-AKI is based on the serum creatinine increase. The usual formulas for estimating glomerular filtration rate (GFR) are not validated in this population. The incidence of P-AKI with respect to total AKI cases has decreased in the last three decades from 25% in 1980s to 9% in 2000s at our centre. During the first trimester of gestation, AKI develops most often due to septic abortion or hyperemesis gravidarum. Septic abortion related AKI with respect to total AKI decreased from 9% to 5% in our study. Prevention of unwanted pregnancy and avoidance of septic abortion are keys to eliminate abortion associated AKI in early pregnancy. However, we have not seen AKI on account of hyperemesis gravidarum over a period of 33 years at our center. In the third trimester, the differential diagnosis of AKI in association with pregnancy specific conditions namely preeclampsia/HELLP syndrome, acute fatty liver of pregnancy and thrombotic microangiopathies of pregnancy (P-TMA) is more challenging, because these 3 conditions share several clinical features of thrombotic microangiopathy which makes the diagnosis very difficult on clinical grounds. It is imperative to distinguish these conditions to make appropriate therapeutic decisions. Typically, AFLP and HELLP syndrome improve after delivery of the fetus, whereas plasma exchange is the first-line treatment for pregnancy associated thrombotic microangioathies (P-TMA). We observed that preclampsia/eclampsia is the most common cause of AKI in late third trimester and postpartum periods followed by puerperal sepsis and postpartum hemorrhage. Pregnancy-associated thrombotic microangiopathies (aHUS/TTP) and AFLP are rare causes of AKI during pregnancy in developing countries.

PE/E was the commonest cause of P-AKI in our study, similar to the situation in developed countries. Post-partum hemorrhage was the second-most common (21.5%) cause. Puerperal sepsis contributed to AKI in one-fourth of pregnant women. P-TMA was not recorded in this study and AFLP was an uncommon cause of P-AKI in our country. Renal function returned to normal in all patients with P-AKI due to pregnancy-specific disorders. However, perinatal mortality was high despite the good prognosis of P-AKI.

Human immunodeficiency virus (HIV) infection can cause a broad spectrum of renal diseases. However, there is paucity of Indian data on the patterns of renal lesions in HIV-seropositive patients. The aim of the present study was to delineate the spectrum of renal lesions in HIV/acquired immunodeficiency syndrome patients. In this prospective study, all HIV-positive patients of both genders aged >18 years were screened for renal disease. Patients with proteinuria of more than 1 g/24 h were subjected to renal biopsy. A total of 293 HIV-positive patients were screened; of these, 136 (46.4%) patients found to have renal involvement. Dipstick-positive proteinuria of 1+ or more was observed in 112 (38.2%) patients, and 16 (14.2%) patients had proteinuria of more than 1 g/24 h. Renal biopsy in 14 cases revealed glomerulonephritis (GN) in 12 (85.7%) (isolated GN in 4 [28.5%] and GN mixed with chronic TIN in 8 [57.1%]) patients. These include mesangioproliferative GN in 5 (35.7%), membranoproliferative GN in 2 (14.2%), focal segmental glomerulosclerosis in 2 (14.2%), diffuse proliferative GN in 2 (14.2%), and diabetic nephropathy in 1 (7.1%) patients. Chronic interstitial nephritis was noted in 10 (71.42%) (superimposed on GN in 8 [57.1%], isolated in 2 [14.2%]) patients. Granulomatous interstitial nephritis was seen in 3 (24.1%) cases. GN and chronic interstitial nephritis were noted in 85.7% and 71.42% of patients, respectively, mostly superimposed on each other. Mesangioproliferative GN was the most common glomerular lesion, but classical HIV-associated nephropathy was not observed.

No abstract

Background: Acute Kidney Injury (AKI) is a common clinical syndrome in hospitalized patients, especially in intensive care units and is a strong risk factor for development of Chronic Kidney Disease (CKD). AKI is a common association in patients admitted for Acute Decompensated Heart Failure (ADHF). AKI is an independent predictor of mortality and poor long term outcome in patients presenting with ADHF. Presently available diagnostic tests in particular serum creatinine, are not helpful in early detection of AKI. Thus a diagnostic tool which can help in early detection of AKI, differentiate various types of AKI, grade the severity of AKI, and suggest appropriate management strategy in patients with ADHF, is need of the hour. Objectives:To analyze role of urine microscopy & urinary biomarkers (N-Acetyl-beta-D-Glucosaminidase, NAG; and Kidney injury molecule type 1, KIM-1) in early detection of AKI and its differentiation into pre-renal and ATN variety in patients admitted with a clinical diagnosis of ADHF. Materials and Methods: 40 patients of ADHF with AKI, along with 25 controls (ADHF without AKI) were studied from January 2019 to December 2019. Urine microscopy with sediment analysis and measurement of urinary biomarkers were done. Results: Urine microscopy helped in differentiation of pre-renal AKI from ATN. The role of urinary sediment examination in risk stratification of AKI did not show a significant correlation between presence of granular casts and three stages of AKI with a P value of 0.561. Levels of urinary KIM-1 and NAG were higher in ADHF with AKI cases as compared to controls with a significant P value of <0.0001 for KIM-1 and 0.003 for NAG. Levels were also higher in cases whose samples were taken within 24 hours of symptom onset of AKI, with a highly significant p value of <0.0001 and 0.001 for KIM-1 and NAG respectively. However urinary biomarker levels did not help in risk stratification of the patients. The correlation of three stages of AKI with urinary levels of KIM-1 and NAG had a P Value of 0.74 and 0.504 respectively. ROC of NAG and KIM-1 were plotted. AUC calculated for KIM-1 was 0.998, for NAG was 0.718 and for the combination was 0.724. There was a significant difference between AUC of KIM-1 and NAG with a p value of <0.001. There was also a significant difference between AUC of KIM-1 and combination of KIM-1 and NAG with a p value <0.001. Conclusions:Urine microscopy is a readily available & inexpensive tool which can help in differential diagnosis of AKI into pre-renal AKI and ATN variety; so that correct therapy can be initiated in time but may not always help to risk stratify patients. The two urinary biomarkers analyzed (KIM-1 and NAG) are useful in early detection of AKI in ADHF patients, however their combination did not have any added advantage of early diagnosis.

Conclusions: We developed a method for virtually continuous measurement of urine flow in the operating theatre. We found that urinary PO 2 provides a relatively robust estimate of medullary PO 2 , but this relationship is confounded by the simultaneous presence of systemic hyperoxia and low urine flow. We observed that during CPB urine flow increases and urinary PO 2 decreases. Thus, it is probable that the best time to use urinary PO 2 to detect renal medullary hypoxia and risk of post-operative AKI is when a patient is on CPB.

Comparing biopsies in elderly and younger adults, elderly individuals were more likely to be hypertensive (83.8% versus 46.2%, p<0.001). Indications for biopsy were not significantly different between elderly and younger adults (all p >0.05): proteinuria and hematuria (49.5% vs. 50.2%), nephrotic syndrome (27.5% vs. 25.4%), isolated proteinuria (22.1% vs. 22.2%), isolated microscopic or macroscopic hematuria (0.9% vs. 0.8%), chronic renal impairment (0 vs 0.8%) and acute kidney injury (0 vs. 0.6%).

No abstract