Contrast-induced Nephropathy among Patients Administered with Contrast Material at a Tertiary Care Centre: A Descriptive Cross-sectional Study.

Introduction: Administration of an intravenous contrast medium, which is used in various routine hospital procedures, can lead to the development of nephropathy in some patients. This contrast-induced nephropathy is one of the most common reasons for hospital-acquired acute kidney injury. This study aimed to find out the prevalence of contrast-induced nephropathy among patients administered with contrast material at a tertiary care centre. Methods: This descriptive cross-sectional study was conducted from 4 March 2022 to 23 May 2022 at a tertiary care centre after taking ethical approval from the Institutional Review Committee (Reference number: 0812202106). Patients administered with an intravenous contrast medium for diagnostic imaging were included in the study. Data including sociodemographic variables and renal function test results were collected. A convenience sampling method was used. Point estimate was done and 95% Confidence Interval was calculated. Results: Among 174 participants, contrast-induced nephropathy was found in 86 (48.31%) (48.24-48.39, 95% Confidence Interval). Conclusions: The study showed that the prevalence of contrast-induced nephropathy was higher than findings from other studies done in a similar setting. Keywords: contrast material; kidney disease; prevalence.

Pneumonia in Patients with Chronic Kidney Disease Admitted to Nephrology Department of a Tertiary Care Center: A Descriptive Cross-sectional Study.

INTRODUCTION: Chronic Kidney Disease is an independent risk factor for pneumonia. The risk of hospitalization, Intensive Care Unit and ventilator requirement, in-hospital death is high in pneumonia patients with chronic kidney disease. This study aims to find the prevalence of pneumonia in patients with chronic kidney disease admitted to nephrology department of a tertiary care center. METHODS: A descriptive cross-sectional study was conducted among all the hospital records of pneumonia patients with Chronic Kidney Disease admitted to the Nephrology department between April 2019 and April 2021. Ethical clearance was obtained from the Institutional Review Committee of same institute (Reference number: 0505202106). Statistical Package for the Social Sciences version 20 was used for analysis. Point estimate at 95% Confidence Interval was calculated along with frequency and proportion for binary data. RESULTS: Of the total 407 patients with Chronic Kidney Disease, 78 (19.1%) (95% Confidence Interval= 15.28-22.92) had pneumonia. Among the 78 pneumonia patients, 17 (21.8%) were Stage 3, 13 (16.7%) Stage 4 and 48 (61.5%) Stage 5 of chronic kidney disease. Forty Seven (60.3%) required Intensive Care Unit (ICU), 19 (24.4%) required ventilator and 22 (28.2%) of the patient expired in hospital. The most commonly isolated organisms were Severe Acute Respiratory Syndrome Coronavirus 2 which was 13 (16.6%) followed by Strepotococcus pneumoniae which was 8 (10.2%). CONCLUSIONS: The prevalence of pneumonia in Chronic Kidney Disease was observed higher in our study compared to other studies.

Association Between Dyslipidemia and Serum Level of 25-Hydroxyvitamin-D in Early Chronic Kidney Disease, Not on Dialysis: An Observational Cross-Sectional Study from the Himalayan Country.

BACKGROUND: Patients with CKD have a higher prevalence of dyslipidemia and hypovitaminosis than the normal population. Recent studies in the general population have shown a potential link between 25(OH)D and dyslipidemia. However, such evidence in the early CKD population, especially in the Nepalese setting, is lacking. Thus, the present study aimed at investigating the status of 25(OH)D and dyslipidemia in the early CKD patients, and further to establish an association between 25(OH)D and lipid profile. PATIENTS AND METHODS: In this cross-sectional study, we analyzed 136 clinically stable non-dialyzed CKD patients. 25(OH)D and lipid profile were evaluated as a core variable, and their direction and magnitude of a relationship were evaluated. RESULTS: The estimated prevalence of dyslipidemia was 49.3%, and 63.2% population had a deficiency of 25(OH)D level. Compared with the patient with normal 25(OH)D level, the patient with deficient 25(OH)D level had a significantly higher level of LDL-c (P=0.04) and lower level of HDL-C (P=0.048). Serum 25(OH)D level was significantly lower in dyslipidemic patients than non-dyslipidemic patients (P=0.015). Regression analysis demonstrated a significant inverse relationship between serum 25(OH)D levels and LDL-c (ß=-1.5; P=<0.001), and TC levels (ß=-1.4;P=0.003), and the association remained unchanged with further adjustment for age, sex, HTN, DM, serum albumin and eGFR. CONCLUSION: Our study unveiled a high rate of dyslipidemia and hypovitaminosis in a considerable number of early CKD patients. Low serum level of 25(OH)D was significantly correlated with a higher rate of dyslipidemia. These findings indicate some evidence for 25(OH)D level as a marker of dyslipidemia prediction, and that decrease in serum level of 25(OH)D is associated with increased serum level of LDL and TC; it could increase the risk of cardiovascular disease. Therefore, early recognition and timely management of hypovitaminosis and dyslipidemia is vital to prevent an inevitable cardiovascular event.

Prevalence of abnormal serum 25-hydroxyvitamin D and its association with hemoglobin level in pre dialysis CKD patients: a cross-sectional study from Himalayan country.

BACKGROUND: CKD has been recognized as risk factors for 25(OH) D deficiency, and Low levels of 25(OH) D have been suggested to be a trigger factor of decreased level of Hb. However, there is lack of information about the magnitude of 25(OH) D deficiency and Hb level in Nepalese CKD patients. Therefore, the aim of present study was to investigate the prevalence of abnormal 25(OH) D in non-dialyzed CKD patients, and further to examine its association with Hb level. METHODS: In this cross-sectional study, we examined 172 clinically stable patients with an eGFR at CKD stage2-5 not on dialysis. Serum 25(OH) D, Hb, levels were evaluated as a core variables and the other variables such as age, sex, co-morbidities (HTN, DM), eGFR, Hb, iPTH, serum phosphate, albumin, calcium, and phosphate level were evaluated as a covariates. Serum 25(OH) D, Hb levels and the factors associated with 25(OH) D level were evaluated. RESULTS: The estimated prevalence of abnormal 25(OH) D metabolite (< 30 ng/mL) in this predialysis patients were (87.8%), with 32 and 55.8% deficiency and insufficiency 25(OH) D metabolite, respectively. On regression analysis, serum 25(OH) D was positively associated with male subjects (P = 0.02), serum albumin(P = 0.002), and eGFR (P = 0.042), while inversely associated with age (P = 0.006), iPTH(P = 0.025). Hb concentration was found to be positively correlated with 25(OH) D (P < 0.05) in both univariate as well as in multivariate analysis. CONCLUSION: A high prevalence of abnormal 25(OH) D metabolite was observed in early CKD patients. Our study shows that lower level of 25(OH) D level are associated with lower level of Hb and higher level of iPTH, and could play a role in the development of anemia and hyperparathyroidism.

Important role for macrophages in induction of crescentic anti-GBM glomerulonephritis in WKY rats.

BACKGROUND: A crucial role for CD8(+) cells in induction of crescentic anti-glomerular basement membrane (GBM) glomerulonephritis (GN) in WKY rats was demonstrated in studies showing that depletion of CD8(+) cells completely suppressed glomerular accumulation of monocytes/macrophages (Mo/Mphi), crescent formation and proteinuria. Because these studies did not definitively identify CD8(+) cells as the cause of tissue injury, we examined the roles of Mo/Mphi in the development of anti-GBM GN. METHODS: We examined correlations between the amount of urinary protein and the numbers of glomerular CD8(+) cells or Mo/Mphi in rats after administrating different doses of anti-GBM antibody (5.0, 7.5, 10.0 and 25.0 microl/100 g body weight). The roles of Mo/Mphi in induction of GN were examined in animals by depleting Mo/Mphi in the glomerulus. To do this, rats were injected intravenously with liposome-encapsulated dichloromethylene diphosphonate (liposome-MDP) from day 3 to day 7 after anti-GBM antibody injection and they were then sacrificed at day 8. RESULTS: Liposome-MDP treatment significantly reduced the number of ED-1(+) Mo/Mphi accumulated in glomeruli from 32.1 +/- 1.2 to 1.4 +/- 0.3/glomerular cross-section (mean +/- SD, P < 0.01), and the amount of urinary protein from 103.8 +/- 19.8 to 31.8 +/- 15.9 mg/day (P < 0.01), as well as the incidence of crescentic glomeruli from 91.3 +/- 2.7 to 23.3 +/- 7.6% (P < 0.01) at day 8. This treatment also reduced the number of CD8(+) cells accumulating in the glomeruli from 5.4 +/- 0.7 to 0.5 +/- 0.1/glomerular cross-section (P < 0.01). Upregulation of glomerular intercellular adhesion molecule 1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) mRNA expression was suppressed by Mo/Mphi depletion. CONCLUSION: These results indicate that Mo/Mphi play an important role in the induction of crescentic anti-GBM GN and glomerular injury.

Involvement of endothelial cell adhesion molecules in the development of anti-Thy-1 nephritis.

To study an involvement of glomerular endothelial cells in the development of anti-Thy-1 nephritis, we examined the expression of endothelial cell adhesion molecules during the course of this model. Ribonuclease protection assay elucidated that expression of mRNA for intercellular adhesion molecule-1 (ICAM-1) was markedly enhanced in the glomeruli with a peak at 2 h (6.5-fold, p < 0.05) after the anti-Thy-1 antibody injection when mesangial cell lysis was recognized and IL-1beta mRNA expression was induced in the glomeruli. The glomerular ICAM-1 was predominantly localized in the endothelial cells and was intensely immunostained at day 1 in the glomerular endothelial cells. In contrast, platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin mRNA expression increased gradually with a peak at day 6 (2.6-fold (p < 0.05) and 4.2-fold (p < 0.05), respectively) in the glomeruli with mesangial proliferative lesion. PECAM-1 was also immunolocalized in the glomerular endothelial cells and the immunoreactivity was greatly enhanced at day 6. Glomerular expression of vascular cell adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 (E-selectin) was unchanged at a low level during the course of anti-Thy-1 nephritis. Blocking of ICAM-1 by administration of anti-ICAM-1 antibody showed significant decrease in the number of polymorphonuclear leukocytes accumulating in the glomeruli by 45.7% (9.4 +/- 0.2 vs. 5.1 +/- 0.1 per glomerular cross section, p < 0.01) at 2 h. These results suggest a significant involvement of glomerular endothelial cells in the development and repair of anti-Thy-1 nephritis via direct or indirect intercellular interactions between mesangial cells and glomerular endothelial cells.