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Hypertension is prevalent in 35%-46% of the general population; 1% of them experience accelerated hypertension. Among patients with accelerated hypertension, acute worsening of renal functions occur in 22%-55%. Morbidity and mortality rates are high. Partial renal recovery is seen in some, while others rapidly progress to end-stage renal disease.
Patients who presented with accelerated hypertension, renal dysfunction, and had undergone renal biopsy were evaluated and their clinical profile was analyzed. Those who became dialysis dependent were excluded from further follow-up. Study outcome were blood pressure control, renal functions, requirement of renal replacement and mortality.
Of the 30 patients evaluated, age at presentation was 41.2 ± 15.46 years and 26 (86.7%) were males, 10 (33%) had presented with nonspecific complaints. Mean duration of hypertension and blood pressure were 21.93 months and 196 ± 20.8/129 ± 12.4 mmHg, respectively. Glomerulonephritis and hypertensive nephrosclerosis had similar characteristics except proteinuria (
= 0.04). Average follow-up (
= 25) duration was 3.69 years (range 0.05-9.6). At the end of study, 6 were dialysis dependent, while in others, mean e-GFR was 23.96 ml/min/1.73 m
. Poor renal prognosis was predicted by glomerulonephritis (relative risk-4.6) and degree of interstitial fibrosis. Five-year patient and renal survival were 94.4% and 71.9%, respectively.
Accelerated hypertension occurs among patients with both primary and secondary hypertension. It leaves permanent renal sequelae. Though some patients recover renal function partially, further progression is rapid, especially among those with chronic glomerulonephritis.
Accelerated hypertension occurs among patients with both primary and secondary hypertension. It leaves permanent renal sequelae. Though some patients recover renal function partially, further progression is rapid, especially among those with chronic glomerulonephritis.
Despite high rates of morbidity and mortality in patients with contrast-induced nephropathy (CIN), there is no consensus regarding prevention of this well-known complication of contrast media use. One agent that has been widely used in this regard is N-acetyl cysteine (NAC). Nevertheless, its efficacy is still controversial. The aim of this study was to assess the efficacy of NAC, both in the oral and intravenous forms, for the prevention of CIN.
This study is a double-blind randomized placebo controlled clinical trial. We randomized 434 adult patients with chronic kidney disease (constant serum creatinine ≥1.5 mg/dL) who were candidates for coronary angiography/plasty. The patients were categorized into three groups. One group received 1,200 mg NAC intravenously half an hour before the procedure and oral placebo starting 3 days before angiography. The second group received oral NAC 600 mg twice daily for 3 days, starting the day before the intervention and intravenous placebo half an hour before intervention. The third group received both oral and intravenous placebo. CIN was defined as a 25% relative increase in serum creatinine from baseline value, 48 h after use of contrast medium.
Of the 434 patients, 149 received intravenous NAC, 145 received oral NAC, and the remaining 140 received placebo. The incidence of CIN in the three groups was 6.1%, 7.6%, and 10.8%, respectively (
= 0.34).
In patients with chronic kidney disease, neither intravenous nor oral NAC is superior to placebo for preventing CIN.
In patients with chronic kidney disease, neither intravenous nor oral NAC is superior to placebo for preventing CIN.
Visceral fat area (VFA) is known to increase after initiation of peritoneal dialysis (PD). However, the factors contributing to the increase in VFA in long-term PD patients have not been sufficiently elucidated. The present study investigated factors that affect VFA in patients who continue PD for ≥3 years.
Twenty patients (63.1 ± 10.3 years, 9 men, 11 diabetic patients) between January 2008 and January 2015 were included. VFA, subcutaneous fat area (SFA) and waist circumference at initiation and follow-up were measured at the level of the umbilicus by computed tomography using an image analysis system. Change in VFA was defined as the value obtained by dividing VFA at the final follow-up by that at the initiation. Firsocostat clinical trial The correlations between clinical parameters at initiation and changes in VFA were analyzed.
There was no significant change in body weight (57.6 ± 10.4 vs 58.3 ± 7.8 kg,
= 0.296) during the mean final follow-up period of 55 ± 13 months, although VFA increased significantly (103.6 ± 39.2 vs 122.6 ± 38.3 cm
,
= 0.030). Although subcutaneous fat area (SFA) did not change (124.7 ± 52.3 vs 124.5 ± 49.2 cm
,
= 0.989), waist circumference increased significantly (79.4 ± 8.4 vs 83.7 ± 6.9 cm,
= 0.010). SFA (r = -0.735, P < 0.001), waist circumference (r = – 0.644,
= 0.002), high-density lipoprotein cholesterol (HDL-C) (r = 0.487,
= 0.029), and age (r = 0.507,
= 0.023) correlated significantly with changes in VFA.
VFA might increase with long-term PD in patients with end-stage kidney disease who have high HDL-C, small SFA, and small waist circumference at initiation.
VFA might increase with long-term PD in patients with end-stage kidney disease who have high HDL-C, small SFA, and small waist circumference at initiation.
Renal failure occurring in the setting of cirrhosis increases mortality by more than threefold. Serum creatinine, the conventional marker for renal dysfunction has inherent limitations in identifying and categorizing renal dysfunction in patients with chronic liver disease (CLD). Neutrophil gelatinase associated lipocalin (NGAL) is a novel biomarker which gets upregulated as early as 2-6 hours following the insult to renal tubules. In this study, we aim to check the utility of uNGAL to identify the different phenotypes of renal dysfunction in patients with CLD. We also intend to assess the utility of NGAL to predict 90-day transplant-free survival in patients with CLD.
A total number of 120 adult patients, with cirrhosis of liver were recruited. Those with pre-existing renal parenchymal disease, receiving nephrotoxic medications, spontaneous bacterial peritonitis, septic shock, proteinuria, hematuria, urinary tract infection and anuria were excluded. Urine samples for NGAL was measured at admission and at 48 hours thereafter.