Pulmonary hypertension (PH) is a recently recognized complication of chronic kidney disease (CKD), especially in end-stage renal disease. It has prevalence estimates of 30%–50% and is an independent predictor of increased mortality in CKD patients. The aim of this study is to analyze the prevalence of PH in patients with CKD, its severity in different stages of CKD, and risk factors for it. One hundred and eight patients with CKD treated at Karnataka Institute of Medical Sciences, Hubli, Karnataka, between January 1, 2014, and June 30, 2015, were selected. Clinical evaluation and relevant investigations including echocardiography were done. Follow-up echocardiography was done at 3 and 6 months and assessed. The mean age of studied population was 43.53 ± 14.63 years. Sex ratio was 2.72:1 (male:female). PH was present in 47 of 108 (43.5%) cases at beginning, 41 of 83 (491.4%) at 3 months, and 32 of 64 (50%) at 6 months. The prevalence and severity of PH increased with progression of CKD stage, although not statistically significant. Heart failure with reduced ejection fraction and heart failure with preserved EF were significantly higher among PH group compared to non-PH group (P < 0.01). Mean hemoglobin in PH group was significantly lower, compared to non-PH group (P < 0.01). Mean interdialytic weight gain and central venous pressure were higher among PH group than non-PH group. Higher calcium phosphate product ≥50 was more prevalent in PH group than in non-PH group. The majority of them had moderate PH at the beginning of the study which remained same, despite being on hemodialysis. PH is a common complication in CKD patients with prevalence of 43.5%–50%. Left-sided heart failure, anemia, fluid retention, and increased calcium phosphate product are the risk factors for developing PH.

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Abnormal primary hemostasis is believed to be the most significant contributor to uremic bleeding. This study aimed to describe the prevalence and profile of primary and secondary hemostatic disorders in patients with chronic kidney disease (CKD) Stages 4 and 5 and to determine their association if any, with degree of uremia. Stages 4 and 5 predialysis CKD patients attending nephrology outpatient clinic were prospectively recruited and the following bleeding parameters were measured in all patients: platelet count, bleeding time (BT), Factor VIII assay, von Willebrand factor antigen (vWF:Ag), vWF:ristocetin cofactor activity (vWF:RCo), ratio of vWF:ristocetin cofactor activity to vWF antigen (vWF:RCo/vWF:Ag), prothrombin time (PT), and activated partial thromboplastin time (aPTT). Forty-five patients (80%, males) with a mean age of 39.4 years, 82% (n = 37) in Stage 5 CKD, were recruited for the study. The prevalence of thrombocytopenia was significantly higher among patients from West Bengal (15/26, 57.7%) compared to other study patients (2/19, 10.5%; P = 0.001); however, all had macrothrombocytes with normal BT, suggestive of the Harris syndrome. Factor VIII, vWF:Ag, vWF:RCo, vWF:RCo/vWF:Ag ratio, BT, PT, and aPTT were abnormal in 0 (0%), 0 (0%), 0 (0%), 4 (8.8%), 1 (2.2%), 7 (15.6%), and 5 (11.1%) patients, respectively. Except for thrombocytopenia, the prevalence of hemostatic abnormalities did not differ between CKD Stages 4 and 5. Hemostatic abnormalities are uncommon in Stages 4–5 CKD and except for thrombocytopenia, are not associated with degree of uremia. Constitutional macrothrombocytopenia is associated with normal BT even in CKD.

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The epidemiological pattern of acute kidney injury (AKI) in tropical countries during monsoon reflects infectious disease as the most important cause. AKI is a confounding factor and may be overlooked by primary health-care providers and underreported in health statistics. The present study prospectively helps estimate the burden of disease and analyze etiology, clinical profile, and outcome in a tertiary care hospital of a metropolitan city in a tropical country. The study period included monsoon season of 2012 and 2013, a total of 8 months. AKI staging was done as per the AKI Network (AKIN) criteria. Patients were treated for primary disease. Renal replacement therapy (RRT) was given as required. Patients were followed up during hospitalization till recovery/death. Out of a total of 9930 admissions during this period, 1740 (17.52%) were for infections and 230 (2.31%) had AKI secondary to infectious diseases during monsoon. The incidence of AKI (230/1740) in infectious diseases during monsoon was 13.21%. The study population (n = 230) comprised 79.5% of males and the mean age was 40.95 ± 16.55 years. Severe AKI: AKIN Stage III was seen in 48.26% of patients and AKIN Stage I in 41.74%. The most common etiology of AKI was malaria (28.3%) followed by acute gastroenteritis (23%), dengue (16.5%), leptospirosis (13%), undifferentiated fever (10.4%), more than one etiology (5.4%), and enteric fever (3.5%). RRT was required in 44.78% of patients. Requirement for RRT was maximum in patients with more than one etiology followed by leptospirosis, malaria, dengue, and least in typhoid. The overall mortality was 12.17%. In multivariate analysis, vasopressor support and assisted ventilation were risk factors for mortality.

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Exercise-induced rhabdomyolysis (EIR) is an uncommon cause of severe rhabdomyolysis and a very rare cause of acute kidney injury (AKI). A prospective observational study of 25 patients diagnosed with EIR was conducted in a multispecialty hospital in Dubai, from 2009 to 2015. Five out of 25 patients experienced AKI necessitating temporary renal replacement therapy. The initial presentation, biochemical parameters, and clinical course of patients were monitored, to understand epidemiology and risk factors for the development of AKI. There was male preponderance (4 out of 5 patients), higher rate of systemic symptoms (all 5 patients) versus 60% in NRAKI), oligo-anuria (all 5 patients), compartment syndrome (3 out \of 5) and severe dehydration seen in patients with RAKI group. On laboratory evaluation, there was higher rise in creatinine kinase (CK) enzyme, serum and urine myoglobin levels impaired renal function on presentation, hyperuricemia, high D-dimer level, PCV of more than 55%, found to be associated with RAKI as compared to NRAKI group. Hematuria by positive urine dipstick with absent red blood cells on urinalysis, is an insensitive tool as was present in only 62% and 43% of RAKI and NRAKI groups, respectively. It was also observed that delayed pesentation for medical care, metabolic acidosis, were commonly associated with AKI. All patients with RAKI required RRT for a comparable period of time (3–4 weeks). In all of them, no deterioration or relapse reported on follow-up of 3 months.

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Renal transplant recipients are at a higher risk of malignancy. We report our experience and the critical differences in the presentation of malignancy in kidney transplant patients performed at our tertiary care center and followed up over the period of 1990–2015. A total of 338 live donor transplants performed in 332 patients were analyzed. Induction immunosuppression was used in 22 cases with interleukin-2 (IL-2) receptor antibody. Overall 299 patients were continued on calcineurin inhibitor (CNI)-based triple drug immunosuppression, 33 were off CNI with 13 of them receiving sirolimus additionally. A total of 16 malignancies including post transplant lymphoproliferative disease (5), oral cancer (5), lung cancer (2), hepatobiliary cancer (2), colon cancer (1), and skin cancer (1) were diagnosed in 15 patients. Over the 26-year follow up, 138 patients died of whom 12 died due to cancer. Cancer occurred in 4.7% of patients but accounted for 9.4% of deaths. Oral cancer occurred after a significantly longer latency of over 10 years (212 vs. 94 months, P = 0.00652). Despite the longer latency, oral cancer patients were younger at diagnosis (44.0 vs. 52 years, P = 0.01016) and had better outcome (Fisher's exact test, P = 0.0275). This was despite a longer overall follow-up for the oral cancer patients, reflecting the better outcome for these patients (24 vs. 4 months, P = 0.0278). This might be the result of relatively early diagnosis of oral cancers.

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Mushroom poisoning is a rare cause of acute kidney injury. Here, we present a case with presumed Amanita nephrotoxic syndrome, a first of its kind from the Indian subcontinent.

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Mortality is substantially elevated in patients on chronic kidney disease in comparison to general population. In this study, we observed the mortality rate in relation to risk factors including low serum bicarbonate level, coronary artery disease (CAD), and dialysis modality in patients on dialysis during a median follow-up time of 60 months. We studied 96 dialysis patients, 62 males and 34 females, on mean age 62.1 ± 14.27 years old. The treatment modalities which were applied were predilution hemodiafiltration (HDF, n = 76), and peritoneal dialysis (PD, n = 20). We performed Kaplan–Meier curves and a Cox-regression analysis to investigate significant risk factors for mortality including hypertension, diabetes mellitus, smoking, bone disease defined by intact-parathormone, serum albumin, serum bicarbonate levels < or >22 mEq/L, dialysis modality, and the existence of CAD. Cox-regression analysis revealed a significant impact of serum bicarbonate levels <22 mEq/L on mortality in combination to dialysis modality and CAD. The prevalence of CAD on mortality was found significant (log-rank = 5.507, P = 0.02). Furthermore, the impact of dialysis modality on mortality was shown significant (log rank = 22.4, P = 0.001), noting that during the first 28–30 months from the treatment initiation, the survival was better for PD; but then, the mortality was significantly increased comparatively to HDF. Uncorrected metabolic acidosis and CAD were shown as independent significant predictors for mortality in patients on renal replacement therapy. PD may provide worse survival after 2–2.5 years of treatment initiation than HDF.

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Antiphospholipid syndrome (APS) associated nephropathy is a distinct clinical entity and can occur in patients with systemic lupus erythematosus (SLE) independent of or associated with lupus nephritis. Associated APS nephropathy in a patient with lupus predicts poor renal outcome, especially if left untreated. Recognizing a coexistent APS nephropathy in a patient with lupus nephritis is of utmost importance. Here, we present a patient with severe lupus nephritis with antiphospholipid antibodies (aPLs) who had no thrombotic manifestations of APS clinically. On renal biopsy, she was found to have APS nephropathy. Remission was achieved after 3 months of anticoagulation and immunosuppression. This case illustrates the importance of renal biopsy in a patient of SLE with aPLs. Renal biopsy often alerts a treating rheumatologist of the presence of thrombotic involvement in such patients, thereby altering the treatment of such patients.

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A 46-year-old male presented with left flank pain and was found to have left nephromegaly with renal vein and inferior vena cava (IVC) thrombus. On hematological evaluation, he had leukocytosis and thrombocytopenia. Further evaluation revealed acute myeloid leukemia (AML). Following initial cytoreductive therapy and supportive care for hyperleukocytosis, he underwent left simple nephrectomy with IVC thrombectomy. Postoperatively, he developed massive thrombosis of infrahepatic IVC with renal failure. Renal venous thrombosis as a rare presentation of AML in adults with leukemic hyperleukocytosis has not been reported. In the absence of clear guidelines, early diagnosis and management are desirable.

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Collapsing glomerulopathy (CG) is a distinct histopathologic pattern of glomerular injury characterized by global/segmental wrinkling of the glomerular basement membrane with podocyte hyperplasia and hypertrophy along with tubulointerstitial changes. There is no specific treatment for CG due to etiological heterogeneity, and newer insights into the pathogenesis may lead to the development of targeted therapy. The most common form of CG is the primary or idiopathic followed by secondary (due to viral infections, autoimmune disease, drugs, etc.) and genetic causes. Thrombotic microangiopathy (TMA) is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ failure of variable severity. We here present two young women with preeclampsia who presented with acute kidney injury, anemia, and schistocytes in peripheral smear suggestive of TMA. Renal biopsy showed interesting histopathology of CG in addition to TMA in the first patient and CG alone in the second. Both the patients received supportive therapy while the first patient also received plasmapheresis. One patient had complete recovery, and other had partial recovery of renal function at last follow-up. Combined histopathological lesion of CG with TMA has never been reported in postpartum period so far in literature.

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Patients with multiple myeloma (MM) often develop renal manifestations. The majority of cases present as cast nephropathy, amyloid light-chain (AL) amyloidosis, and monoclonal immunoglobulin deposition disease. AL amyloidosis usually involves the glomeruli, blood vessels, and interstitium. It is extremely uncommon to find isolated intratubular deposition of AL amyloid. Our patient presented with rapid worsening of renal function due to isolated intratubular deposition of AL amyloid, where the biopsy revealed amyloid proximal tubulopathy and amyloid cast nephropathy. Our case provides new insights into the complicated pathophysiology of the abnormal light chains in MM. This case is, to our knowledge, the second case of amyloid proximal tubulopathy reported in literature.

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The stomach mechanoreceptors can be stimulated by gastric distension (GD) and through afferent vagal nerve, increased activity of the renal sympathetic pathways. Because renal sympathectomy can abolish the protective effect of ischemic preconditioning, it seems that GD preconditioning can be effective in renal ischemia/reperfusion (I/R) injury. Gastric inflate (8 ml of 37°C water for 20 min) by a latex balloon inserted into the stomach through the fundus; I/R group was subjected to 45 min of bilateral ischemia and 24 h of reperfusion. GD preconditioning decreases blood urea nitrogen, creatinine, kidney damage score, and alkaline phosphatase levels compared to the sham GD group (P < 0.05). GD preconditioning may protect renal I/R injury through anti-inflammatory activity, but this efficacy requires extensive studies on the methods and mechanisms.

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Hypertension is a frequent early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Many mechanisms cause hypertension in ADPKD; however, primary aldosteronism (PA) as a possible manifestation of hypertension in ADPKD is extremely rare. The diagnosis of PA in ADPKD is extremely challenging because multiple renal cysts can mask the identification of adrenal adenomas, and ADPKD is associated with hypertension in majority of cases. Here, we report a unique case of a young lady with ADPKD with hypertension masquerading PA.

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