Background:The prevalence of Hypertension is 29.8% in India and is directly responsible for 57% of all stroke deaths and 24% of all coronary heart disease (CHD) deaths Objective: This study focuses on prevalence of microalbuminuria in hypertension, its correlation with duration and severity of hypertension, and lastly whether microalbuminuria is a useful biomarker for predicting target organ damage. Material & Methods:The study was conducted in MGM Medical College and Hospital Navi Mumbai for a period of 2 years between 2015 to 2017.Patients between 25 -60 years of age, with at least 3 readings of increased blood pressures or known hypertension were studied extensively.Univariate analysis (chi square test) was used to determine the relationship between MA and other variables, and the results were expressed as p values. Results:The overall prevalence of MA in the study was 49% of which 71% were males.40.82% of patients with microalbuminuria were between 41 -50 years of age.There was a strong correlation (p < 0.05) between severity of hypertension and MA as 57.74% patients of Stage-2 JNC-7 classification of hypertension had microalbuminuria.Conclusions: The prevalence of Microalbuminuria, is about 49% among the patients with hypertension.The factors that are positively correlated with microalbuminuria, in the study, are, older age, severity of hypertension.
INTRODUCTION: Severe acute respiratory syndrome coronavirus (SARS-CoV) has mutated over time, affecting its virulence, pathogenicity and disease severity. In December 2019, a new coronavirus (SARS-CoV-2) has emerged causing a disease known as coronavirus disease (COVID-19). The COVID-19 has a broad spectrum of severity ranging from an asymptomatic to a severe acute respiratory syndrome requiring mechanical ventilation. COVID-19 is often more severe in people aged 60 years or more, or those with health conditions like lung or heart disease, diabetes, or conditions that affect the immune system including kidney transplant recipients. In this case series, we presented our experience with 17 kidney transplant recipients who had COVID-19 infection. In India, COVID-19 peaked twice: once between August and November 2020, and again between March and June 2021. Thus, there was paucity of COVID-19 data in kidney transplant recipients in India during these times. MATERIAL AND METHODS: Our case series constituted a retrospective observational study involving 17 kidney transplant recipients who experienced COVID-19 infection from November 2020 to September 2021 at a solitary tertiary care center in Pune. Within our institution, the nephrology team assessed kidney transplant recipients with COVID-19 for appropriate immunosuppression dosing, renal drug clearance when deemed necessary, and overall well-being. Treatment for COVID-19 adhered to institutional protocols. RESULTS: In our case series, majority of the patients (n=13) had COVID-19 in March 2021 to July 2021 and the commonest presenting symptoms were fever and cough. Out of 17 kidney transplant recipients included in this case series, 13 patients survived while 4 patients succumbed to infection. CONCLUSION: An individualized, case-based approach to managing transplant recipients with COVID-19 is crucial for achieving favorable clinical outcomes.
Background The role of T-regulatory cells (Tregs) in inflammatory renal disease is not yet established. We attempted to study peripherally circulating T-cells expressing RORγt+Foxp3+ dynamics in acute kidney injury (AKI) and chronic kidney disease (CKD). Aim To determine the role of T-regulatory cells in AKI and CKD. Research methodology This is a cross-sectional study conducted between January 2019 to January 2021 at a single tertiary care centre in Pune, India. Candidates enrolled in the study were either patients with CKD not on maintenance hemodialysis or newly diagnosed cases of AKI. Kidney transplant recipients, patients with autoimmune diseases like systemic lupus erythematosus (SLE), IgA nephropathy, or those receiving immuno-suppressants were excluded. T-lymphocytes were analyzed using a flow cytometer. Results We studied 80 patients with kidney injury, 40 each belonging to the AKI and CKD study groups and 10 healthy volunteers as controls. The rationale behind having a small control group was to merely get an idea of T helper 17 (Th17):Treg ratio and different immune cell-phenotype profiles in healthy volunteers without kidney injury, diabetes, hypertension or any other risk factors. The ratio of RORγt:Foxp3 was ≤ 1 in these individuals (control group) while this ratio was significantly altered (MFI RORγt:Foxp3 ≥1) in the AKI/CKD study arm. We examined peripherally circulating T-lymphocytes in acute kidney injury and chronic kidney disease, comparing their activity to healthy volunteers. Biopsy-proven kidney injury patients (29/80) were also included in this study. We found that the ratio of RORγt:Foxp3 was altered in patients with kidney injury (acute and chronic) and was statistically significant compared to controls, indicating that injury may be attributed to T-cell dysfunction. Conclusion Our study provides some evidence of T-cell dysfunction in the pathology of kidney injury in acute and chronic kidney disease via activity of Foxp3 and RORγt. We found that there is evidence of altered Th17/Treg activity in kidney injury, more prevalent in acute than chronic, when compared to healthy volunteers.
Graft-site candidiasis is a rare manifestation of invasive fungal infections, with a risk of 1.3% in kidney transplants. The incidence of graft-site candidiasis is 0.1% in renal transplant recipients. Preservation of the renal graft is rarely possible when candidiasis is accompanied by vascular complications.
48-year-old male, Mr. GS, presented with fever, abdominal distension, pedal edema, and reduced urine output since 5 days. There was no history of hematuria, dysuria, foul smelling urine, abdominal tenderness, and passage of fleshy mass during micturition. He is known case of hypertension and type 2 diabetes mellitus. There was no history of stroke, coronary artery disease, and NSAID abuse in the past. His weight was 109 kgs, height 178 cm, and BMI 34.4 kg/m2. His pulse was 88/min; BP was 90/60 mmHg.
Dear Editor, Recurrent intracerebral hemorrhage (ICH) is usually a result of uncontrolled hypertension. It can sometimes coexistwith posterior reversible encephalopathy syndrome (PRES). Herein, we present a kidney transplant recipient (KTR) diagnosed with tacrolimus-associated cerebral vasculopathy leading to recurrent ICH, associated with neither uncontrolled hypertension nor PRES, necessitating drug withdrawal. A 47-year-old deceased donor KTR presented with sudden-onset headache, altered behavior, and focal seizures 2 years post-transplant. Her native kidney disease was presumed to be chronic interstitial nephritis. She was on peritoneal dialysis for 4 years before transplant. She had received induction with equine antithymocyte globulin and was taking the standard triple-drug immunosuppression. Her posttransplant clinical course was uneventful, except for development of posttransplant diabetes mellitus at 3 months following transplant, which was under control with metformin monotherapy. Her blood pressure was always under control. She had no other comorbid illnesses. She was having stable graft function (serum creatinine 0.8 mg/dL). Tacrolimus trough level was 4.6 ng/mL. Computed tomography (CT) of the brain showed ICH with large hematoma (50 × 40 mm) in the left parieto-occipital region with perifocal edema. Past history was significant with two similar episodes of ICH 7 and 15 months ago, affecting the right frontal lobe (30 × 20 mm) and the right temporoparietal lobe (40 × 20 mm) [Figure 1].Figure 1: Computed tomography axial images of the brain showing ICHs at three different time points in the same patient. (a) First episode of ICH affecting the right temporoparietal lobe at 9 months posttransplant (40 × 20 mm). (b) Second episode affecting the right frontal lobe at 17 months posttransplant (30 × 20 mm). (c) Third episode affecting the left parieto-occipital region at 24 months posttransplant (50 × 40 mm). ICH = intracerebral hemorrhageRecurrent ICH can result from uncontrolled hypertension, coagulopathies, arteriovenous malformations, aneurysms, neoplasms, vasculitis, infections (especially, herpes simplex virus encephalitis), PRES syndrome, and amyloid angiopathy. All the three episodes of ICH were associated with neither severe hypertension nor trauma. She was extensively evaluated with CT angiogram, magnetic resonance angiography, and venography. As there was no apparent predisposing cause, drug-induced toxicity was suspected. Tacrolimus was stopped, and she was shifted to low-dose cyclosporine. Cyclosporine trough whole blood level was targeted between 75 and 100 ng/mL. At 12 months follow-up, she is doing well with no further neurological events. Neurotoxicity is one of the common complications of calcineurin inhibitors (CNIs). The severity of symptoms varies from mild and self-limiting to severe and life-threatening. These include tremors, ataxia, agitation, confusion, nightmares, headache, visual disturbances, focal neurological deficits, cortical blindness, altered mental status, encephalopathy, seizures, and coma. These are generally more common with tacrolimus than cyclosporine. Several cases of ICH after solid organ transplantation have been reported, but mostly in the setting of PRES and rarely due to cerebral venous sinus thrombosis. Tacrolimus is well known to precipitate PRES, and ICH is known to occur in PRES.[1] Tacrolimus is also known to induce reversible cerebral vasoconstriction syndrome, thereby precipitating ICH. However, in our patient, the three episodes of ICH were not associated with clinical or imaging evidence of PRES. Blood pressure was moderately elevated in all the three episodes. Neither there was an evidence of coagulopathy, nor she was on coagulation altering medication. After excluding all the common possible causes of ICH, we concluded it as tacrolimus-associated cerebral vasculopathy presenting with recurrent ICH. Stereotactic brain biopsy-proven tacrolimus-associated cerebral vasculitis with distinct microglia activation was initially described in a liver transplant recipient.[2] Later, it was identified that tacrolimus-induced ICH was significantly more common after allogeneic bone marrow transplantation than after solid organ transplantation. Various pathophysiological mechanisms have been proposed. Calcineurin is expressed in several areas of the brain such as cerebral cortex, striatum, substantia nigra, cerebellum, and hippocampus. CNIs, especially tacrolimus, can cause direct endothelial cell injury and alteration of the blood–brain barrier (BBB). Experimental studies conducted in vitro on mouse brain capillary endothelial cells have shown a direct cytotoxic effect of tacrolimus on endothelial cells.[3] It was also confirmed in autopsies.[4] It is also known to induce vasoconstriction through endothelial cell production and release of endothelin, systemic sympathetic stimulation, and reduced nitric oxide production. Systemic and/or renal vasoconstriction with resultant hypertension could lead to reduced cerebral blood flow due to autoregulatory vasoconstriction. In addition, these drugs could reduce cerebral blood flow directly, secondary to cerebral vasoconstriction. The combined effects might lead to increased but complex cerebral vascular instability, with an increased risk of ICH. Disruption of the BBB and the cytotoxic effects on the vascular endothelium result in leakage of fluid into the interstitium, which leads to vasogenic edema. This, in turn, may progress to ICH. Tacrolimus-induced cerebral microbleeds may predispose to symptomatic ICH. Tacrolimus causing ICH secondary to cerebral vasculopathy seems to be a rare event. Only one similar case has been reported in a KTR till date.[5] However, recurrent ICH was never reported in the past. ICH may be a marker of tacrolimus-associated vasculopathy. High index of suspicion and early intervention in the form of drug withdrawal may prevent its recurrence. Although the exact pathogenesis of ICH remains unknown, tacrolimus could play a direct role in the occurrence of this process regardless of the drug levels as it may remain within the therapeutic range. It remains a diagnosis of exclusion after ruling out the common predisposing causes for ICH. This case illustrates that tacrolimus-associated vasculopathy can occur even at the therapeutic level of tacrolimus in the blood and it can predispose to ICH, which can be recurrent. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
A 40-year-old female of Indian origin underwent spousal donor ABO-incompatible (ABOi) kidney transplantation. She was diagnosed to have end-stage kidney disease, around 1 year before transplant and it was presumed to be chronic tubulointerstitial nephritis. The female was detected to have acute hepatitis B, 2 months before transplant. She was a highly-sensitized patient with a prior history of blood transfusion and multiparity. Single-antigen bead assay was positive pretransplant. The removal of anti-human leukocyte antigen donor-specific antibodies and anti-B antibodies in our patient was a multi-step process. Timely initiation of antiviral therapy is crucial to reduce viral load and make the patient fit for transplantation. Despite a multitude of risk factors, our patient underwent successful kidney transplantation with a baseline creatinine of 0.6 mg/dL and excellent graft function.
Background and Objective: Obesity has emerged as a worldwide phenomenon affecting wealthy and middle income groups as well as residents of countries previously considered to be poor.Based on epidemiological data, the higher the BMI, the greater is the risk of developing chronic health problems like Hypertension, Diabetes mellitus, Coronary artery disease, certain cancers, arthritis, central obesity and Cerebrovascular disease.The major weakness of BMI is that it indicates excess body weight and not fat, and more importantly, does not count for the variation in the distribution of fat within the body.Central obesity in patients, predisposes them to major metabolic problems, cardiovascular events, dyslipidemia, and it cannot be measured by BMI alone.Hence, waist circumference (WC) becomes better indicator for central adiposity. Aims & Objectives: To study whether body mass index (BMI) and waist circumference as combined indicators have a better correlation with cardiovascular risk factors in obese individuals than their individual correlation with the risk. Methodology:The study was conducted on 150 patients attending Medicine OPD in a tertiary care hospital.Data in the form of history, clinical examination and blood investigations, mainly lipid profile was collected.Both quantitative and qualitative data were analyzed statistically to study the correlation of combined use of BMI and WC to predict cardiovascular disease.(p-value<0.01),mean TG levels (p-value~0.01),mean HDL level (p-value~0.12),Dyslipidemia (p-value<0.05) and Hypertension (p-value<0.01) were statistically significant in the study population. Results: This is a cohort study having statistically significant correlation of combination of BMI and Waist Circumference and their impact on development of risk factors (dyslipidemia and hypertension) for cardiovascular disease. The mean total cholesterol level Conclusion:The study was based on, calculating BMI and WC together and correlating the risk factors for cardiovascular disease.It is found that cardiovascular disease risk is greater in individuals with higher BMI and waist circumference (WC).The combined use of BMI and WC appeared to be more predictive of cardiovascular disease.Patients with no previous co-morbidities but with increased BMI and WC, had hypertension and dyslipidemiaas compared to those with normal BMI and WC.
Mucormycosis is a progressively invasive disease, with a fatal outcome, on late presentation. A 38-year-old female presented with diabetic ketoacidosis with right eye ptosis and a frozen globe without any signs of inflammation, externally. She underwent transnasal endoscopic debridement of paranasal sinuses and exenteration of the right eye. The histopathology specimen revealed the growth of mucormycosis. She was treated with intravenous (IV) amphotericin B, IV insulin, and extensive debridement surgery, but had an unfavorable outcome due to rapid mucor invasion to the brain.
Pickling paste is used for cleaning stainless steel weld seam heat marks. It is a mixture of hydrofluoric acid (HF) and nitric acid (HNO3) with surfactants and inhibitors. The substance is corrosive, toxic, and irritant. Air respirator and half mask air filter covering nose and mouth are mandatory before handling the pickling paste. This is a case report of a 28-year-old male complaining of sudden onset dyspnea at rest after accidental inhalation of pickling paste fumes. The patient developed acute lung injury and subsequently acute respiratory distress syndrome and was treated with noninvasive ventilation, steroids, and other supportive treatment.
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