albuminuria

Introduction: Hypertensive cardiopathy is the target organ lesion caused by arterial hypertension (HTN) that exhibits the highest morbidity and mortality rates. Although the importance of hemodynamic overload exerted by HTN on the onset of cardiopathy is well established, several non-hemodynamic factors may contribute significantly to its development. Objective: To evaluate the influence of different non-hemodynamic risk factors in the development of hypertensive cardiopathy. Methods: A prospective cohort study was carried out in hypertensive patients assisted at the specialized arterial hypertension physicians’ office of the “Carlos Manuel de Céspedes” Specialty Policlinic attached to the General University Hospital, Bayamo Municipality, Granma Province, Cuba from January 5, 2006 to December 31, 2015. The study included 18-to-55-year-old hypertensive patients with a stage 1 arterial hypertension diagnosis for less than a year1. Results: The multivariate analysis showed a significant and independent relation among the majority of the factors studied and the risk of developing cardiopathy. The major factor was C-reactive protein (HR: 5.020; IC 95%: 3.383-7,448; p<0.005) followed by microalbuminuria (HR: 2.649; IC 95%: 1.932-3.631; p<0.005). The area under the model ROC curve was 0.887 (p<0,005). Conclusions: The results showed that it is possible to estimate the risk of developing hypertensive cardiopathy with the application of the regression model to major risk factors.

Endothelial dysfunction and inflammation play a key role in the pathophysiology of diabetic nephropathy; Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthase, when BH4 is reduced to dihydrobiopterin (BH2), endothelial dysfunction is induced. Purpose: The aim of this study is to evaluate the relationship between the levels of biopterins with albuminuria in type-2 diabetic hypertensive patients. Methods: We studied 30 hypertensive type-2 diabetic patients in whom biopterins levels were measured by reverse phase high performance liquid chromatography with fluorescence detection. Additionally, 24 h urinary albumin excretion was also measured (nephelometry). The levels of biopterins and albuminuria were correlated with the Pearson correlation coefficient. Results: We did not find a significantly correlation between biopterins levels and albuminuria, However, we found a significantly inverse correlation (R= -0.498, p<0.005) between the BH4/BH2 ratio and albuminuria. Conclusion: Our results suggest that the BH4/BH2 ratio instead of biopterins levels may be a marker of nephropathy in hypertensive type-2 diabetic patients.

Background: Chronic Kidney Disease is no longer considered just a health burden today but a major health priority owing to its high treatment costs and poor outcome. World Kidney Day and International Women’s Day in 2018 coincided, thus offering an opportunity to reflect on the importance of women’s health, and specifically their kidney health. The current study aims to identify chronic kidney disease in women through a cross sectional screening in hospital based camp in Varanasi on World Kidney Day. Methods: 138 females attending a health camp were screened for clinical parameters like serum creatinine, random blood sugar, and pregnancy complications. Demographic and anthropometric parameters were noted. Ordinal logistic regression analysis was used to find the predictors of chronic kidney disease stages. Results: The median age of the participants was 36 years. The prevalence of chronic kidney disease was 6.4% with 1.4% of Stage 1, 2.1% of Stage 2, 1.4% of Stage 3 and 1.4% of Stage 4. Women with diabetes were nearly 4 times at a greater risk of developing higher stages of chronic kidney disease compared to women without it. With a unit increase in serum creatinine levels, women were nearly 13 times more likely to develop higher stages of chronic kidney disease. Conclusion: Serum creatinine levels and diabetes were the significant predictors for the development of higher stages of chronic kidney disease. Early screening for kidney diseases in women could reduce the load of health care delivery system that is involved in renal replacement therapies.

Introduction: Chronic kidney disease is a costly and burdensome public health concern. Delayed recognition and treatment of CKD may predispose patients to unfavorable future outcomes and burden the healthcare services. The early detection of disease via screening programs is widely recommended. The present study is a hospital camp-based screening for detecting patients with chronic kidney disease in Varanasi from 2014-18. Methods: The study subjects constituted 436 apparently healthy adults (age ≥18 years) of Varanasi. Information on socio-demographic profile, personal characteristics and clinical investigations were recorded. Stepwise binary logistic regression analysis was applied to find the significant predictors of chronic kidney disease. Results: Median age of the study subjects was 40.5 years. There were 39.7% males and 60.3% females. Chronic kidney disease was found in 23.9% subjects. Underweight, diabetes mellitus, hypertension, smoking status and higher creatinine levels came out as significant predictors of chronic kidney disease. Conclusion: We screened apparently healthy individuals and found very high percentages of chronic kidney disease and its predictors. Henceforth, understanding the preventable and modifiable risk factors of chronic kidney disease becomes a prerequisite to intervene before risk populations reaches to irreversible stages of adverse future outcomes.

We investigated the existence of microalbuminuria in children with corticosteroid-sensitive idiopathic nephrotic syndrome in complete remission. In the study of a series of 18 cases, we noted a clearly different evolution depending on the existence or absence of pathological micro albuminuria. Microalbuminuria appears to be a prognostic discrimination parameter in idiopathic nephrotic syndrome. 

Background: Glomerular hyperfiltration (GH) is a common feature of sickle cell nephropathy (SCN) starting at infancy and represents an early marker of incipient glomerular injury and renal dysfunction. Methods: This study aimed to determine the prevalence and correlates of GH among children (≤ 16 years) with sickle cell disease (SCD) at their steady state, recruited over 6 months at the Pediatric Outpatient Clinic in Al-Sadaqa General Teaching Hospital, Aden, Yemen. Glomerular filtration rate (eGFR) was estimated using the Schwartz formula. Data on clinical history, anthropometry, blood pressure (BP) and laboratory investigations were collected. Results: Of 101 children (mean age 7.2 ± 3.9 years), 65 (64.4%) were males. The prevalence of GH was observed in 36 (35.6%) children, who were significantly older (10.7 ± 3.2 vs. 5.2 ± 2.7 years, p < 0.001) and had a lower fetal Hb level (5 ± 3.3 vs. 9 ± 7.1, p = 0.02). All children were normotensive, but hyperfiltrating children showed significantly higher systolic (97.2 ± 7.3 vs. 89.7 ± 5.2 mmHg) and diastolic pressure (55.1 ± 5.0 vs. 49 ± 4.3 mmHg) (all p < 0.001). Among evaluated children, 25.7% had hyperfiltration alone, whereas 9.9% had an associated microalbuminuria (MA), and no significant difference in eGFR between those with and without MA (158.4 ± 33.7 vs. 160.7 ± 29.8 ml/min/173m2, p = 0.84). Conclusion: This study demonstrated a relatively high prevalence of GH in Yemeni children with SCD that increased with age. Recognition of hyperfiltration and other early markers of nephropathy in this population could help to develop renal protective strategies to prevent progressive loss of kidney function.

Introduction: Sodium-glucose cotransporter 2 inhibitors such as empagliflozin (EMPA) protect against diabetic kidney disease. Prostaglandin E2 (PGE2) the main renal product of cyclooxygenase-2, inhibits vasopressin (AVP)-water reabsorption in the collecting duct (CD). The novelty of this study is that for the first time, we examined if EMPA affects the renal PGE2/EP receptor system and determined if CD responses to EMPA prevent water loss. Methods: Four groups of adult male mice were studied after 6 weeks of treatment: control (db/m), db/m+EMPA (10 mg/kg/day in chow), type 2 diabetic diabetic/dyslipidemia (db/db), and db/db+EMPA. Tubules were microdissected for quantitative polymerase chain reaction (qPCR) and CD water transport was measured in response to AVP, with or without PGE2. Results: Hyperglycemia and albuminuria were attenuated by EMPA. Renal mRNA expression for COX, PGE synthase, PGE2 (EP) receptor subtypes, CD AVP V2 receptors and aquaporin-2 was elevated in db/db mice, but unchanged by EMPA. Urine PGE2 levels increased in db/db but were unchanged by EMPA. AVP-water reabsorption was comparable in db/m and db/m+EMPA, and equally attenuated to 50% by PGE2. In db/db mice, AVP-water reabsorption was reduced by 50% compared to non-diabetic mice, and this reduction was unaffected by EMPA. In db/db mice, AVP-stimulated water transport was more significantly attenuated with PGE2 (62%), compared to non-diabetic mice, but this attenuation was reduced in response to EMPA, to 28%. Conclusion: In summary, expression of renal PGE2/EP receptors is increased in db/db mice, and this expression is unaffected by EMPA. However, in diabetic CD, PGE2 caused a greater attenuation in AVP-stimulated water reabsorption, and this attenuation is reduced by EMPA. This suggests that EMPA attenuates diabetes-induced excess CD water loss.

Introduction: Diabetes mellitus and diabetic nephropathy are the most common causes of end-stage renal disease (ESRD) in developed countries, accounting for about 30% of these cases. Up to 40% of patients with type 2 diabetes with micro albumin uria progress to overt nephropathy and develop ESRD after one to two decades. Albumin uria is the most important indicator of diabetic nephropathy and its progression. Also, hyperuricemia has been suggested as a risk factor for kidney damage, this study was designed to determine the relationship between serum uric acid level and proteinuria in patients with type 2 diabetes.Materials and methods: In this descriptive-analytical and cross-sectional study, data collection was performed among patients with type 2 diabetes referred to the diabetic Center in Gorgan from the years 2015 to 2018. The data collection tool was a two-part questionnaire including demographic and anthropometric characteristics and information about the disease. Serum levels of Uric Acid, Blood Urea Nitrogen (BUN), Creatinine (Cr), Fasting Blood Sugar (FBS) and Hemoglobin A1C (HbA1C) were measured in all patients. 24-hour urine collection was performed for proteinuria, albuminuria, urinary volume, and Cr volume. Patients’ GFR was also calculated using the CKD-EPI formula. Patients were re-evaluated 1 year after the initial evaluation in terms of measured factors and the relationship between serum uric acid and albuminuria, proteinuria, kidney function, and other serum factors were evaluated.Results: Among 823 diabetic patients that were referred to the nephrology center in this study, 90 patients were included. 34 (37.8%) of these patients were men. The age range of patients was between 32 years to 70 years with a mean of 56.31 and a standard deviation of 7.84 years. According to the Pearson correlation coefficient, a direct correlation was observed between uric acid with proteinuria and creatinine levels, and an inverse correlation was observed between uric acid and GFR. But we didn’t find any correlation between uric acid and microalbuminuria.Conclusion: According to the results of this study, the relationship between uric acid level and the severity of nephropathy (based on proteinuria) is proven. It seems that maintaining serum uric acid levels in patients with type 2 diabetes within the normal range and treatment with serum uric acid-lowering drugs may be possible to reduce the progression of diabetic nephropathy and proteinuria.

Chronic Kidney Disease (CKD) is a significant public health issue with a rising prevalence globally. Diabetic kidney disease (DKD), a leading cause of CKD, necessitates improved biomarkers for early detection and effective management. Traditional markers such as serum creatinine, estimated glomerular filtration rate (eGFR), and albuminuria have notable limitations in sensitivity and specificity, especially for early detection. Fetuin-A, specifically its post-translationally modified form (PTM-Fetuin-A), has emerged as a potential novel biomarker for DKD. This study evaluates PTM-Fetuin-A in a cohort of Bulgarian patients with type 1 and type 2 diabetes, assessing its correlation with traditional markers such as albuminuria and eGFR. Significant correlations were observed between PTM-Fetuin-A and these indicators (e.g., Pearson’s r = 0.447, p = 0.025 for albuminuria), highlighting its ability to detect early kidney function decline. Furthermore, PTM-Fetuin-A demonstrated potential as a non-invasive tool for identifying normoalbuminuric DKD, addressing gaps left by conventional biomarkers. By offering additional prognostic value, PTM-Fetuin-A could improve the early diagnosis and clinical management of diabetic patients, reducing the burden of CKD.

Amyloidosis-associated kidney disease commonly manifests with chronic glomerular symptoms including heavy proteinuria predominantly albuminuria. Clinical presentation ranges from full-blown nephrotic syndrome, hematuria, and hypertension to renal failure. In India patients with chronic kidney disease are mainly attributed to hypertension and diabetes but an underlying etiology such as amyloidosis needs to be unearthed and shouldn’t be ignored as an etiology. We report a case of a 60-year-old man with hypertension and hypothyroidism who presented with frothy urine for several years, b/l pedal edema for 15 days. Over the past 3 months, there was a serial increase in creatinine. As per CKD-EPI equation, the patient was CKD-4. As the patient was suspected to be rapidly progressive renal failure; a renal biopsy was planned. Biopsy reports were suggestive of Amyloidosis. Glomerular, vascular, and tubulointerstitial deposition of amyloid was seen. Based on renal biopsy and IHC staining; the patient’s diagnosis was AA-associated secondary renal amyloidosis. Thus in this case renal amyloidosis was an unearthed etiology.