Is the combination of linagliptin and allopurinol better prophylaxis against post-contrast acute kidney injury? A multicenter prospective randomized controlled study.

Background: Patients with diabetic kidney disease (DKD) are at increased risk to develop post-contrast acute kidney injury (AKI). Diabetic patients under dipeptidyl peptidase 4 inhibitors (DPP4Is) experience a lower propensity to develop AKI. We speculated that linagliptin as a single agent or in combination with allopurinol may reduce the incidence of post-contrast AKI in stage 3-5 chronic kidney disease (CKD) patients with underlying DKD.

Sodium-glucose cotransporter 2 inhibitors as the first universal treatment of chronic kidney disease.

In the last five years, the medical community was astonishingly surprised by the sequential large outcome trials that displayed the renal effects of sodium glucose co-transporter inhibitors (SGLT2Is) in type 2 diabetes mellitus (T2DM) patients with or without chronic kidney disease (CKD). This favorable effect was later disclosed in non-diabetic CKD patients. The EMPA-REG OUTCOME trial was the first trial that showed a reduction for the need for dialysis in patients suffering diabetic kidney disease (DKD) by 55%.

Serum sclerostin in acute kidney injury patients.

Background: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI.

Sodium-glucose cotransporter 2 inhibitors as the first universal treatment of chronic kidney disease.

In the last five years, the medical community was astonishingly surprised by the sequential large outcome trials that displayed the renal effects of sodium glucose co-transporter inhibitors (SGLT2Is) in type 2 diabetes mellitus (T2DM) patients with or without chronic kidney disease (CKD). This favorable effect was later disclosed in non-diabetic CKD patients. The EMPA-REG OUTCOME trial was the first trial that showed a reduction for the need for dialysis in patients suffering diabetic kidney disease (DKD) by 55%.

Serum sclerostin in acute kidney injury patients.

Background: Many of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI.

Serum Urate Lowering Therapy Using Allopurinol Improves Serum 25 Hydroxy Vitamin D in Stage 3-5 CKD Patients: A Pilot Study.

Background: Recent studies have demonstrated negative associations of serum uric acid (SUA) with serum 25 hydroxy vitamin D (25 [OH] vit D) among CKD patients.

Objective: The aim of the study was to look for the impact of hypouricemic therapy using allopurinol on serum level of 25 (OH) vit D in CKD patients.

Cases And Methods: Seventy-two CKD stage 3-5 patients were selected to this study.

Vitamin-D deficiency is encountered in almost all egyptian stage 3-5 chronic kidney disease patients in spite of the sunny weather.

Currently, there is no available data about Vitamin D status among Egyptian chronic kidney disease (CKD) patients. This cross-sectional study is looking for the prevalence of Vitamin D deficiency among Stage 3a-5 CKD Egyptian patients and its possible associations. We studied 1624 Stage 3a-5 CKD adults (689 males and 935 females) together with 200 normal control persons.

Impact of hepatitis virus infection on arterial calcification among incident hemodialysis patients.

Background: The impact of hepatitis virus infection on arterial calcification (AC) was not studied.

Objective: To study the prevalence, severity and distribution of AC in incident hemodialysis patients with hepatitis B and C viral infection.

Cases And Methods: 172 stage 5 CKD adults (98 male and 74 female) were included; 58 of them were seronegative for both hepatitis B and C (SN group), 48 were positive for hepatitis B virus infection (HBV group) and 66 were hepatitis C virus positive (HCV group).

Urine albumin and serum uric acid are important determinants of serum 25 hydroxyvitamin D level in pre-dialysis chronic kidney disease patients.

Low serum 25 hydroxyvitamin D (25 OH D) is common among chronic kidney disease (CKD) patients. This cross-sectional study is looking for the different factors associated with serum 25 OH D among pre-dialysis CKD. 1624 adult stage 3-5 CKD patients were studied beside 200 normal control subjects.

Intraoperative Arterial Biopsy in Incident Hemodialysis Patients: Differences Observed.

Introduction: Arterial calcification (AC) is a common complication in chronic kidney disease (CKD) patients that starts to develop before these patients need renal replacement therapy. In these patients, calcification can involve tunica intima or tunica media. This study has looked for the prevalence, severity, and distribution of arterial wall calcification in incident hemodialysis patients through intraoperative arterial biopsy obtained during creation of arteriovenous vascular access for hemodialysis.

Serum 25-hydroxyvitamin D level is negatively associated with serum phosphorus level among stage 3a-5 chronic kidney disease patients.

Background: Serum 25-hydroxyvitamin D (25(OH)D) negatively correlates with serum phosphorus level of stage 3a-5 chronic kidney disease (CKD) patients. So far, no explanation has been provided for this negative association.

Objective: To confirm this negative association and determine if this relationship is mediated through other known co-morbid factors.

Vitamin D deficiency: an unrecognized cause of flank pain.

Loin pain is frequently not associated with any urinary abnormality. Musculoskeletal abnormalities are not uncommon as alternative cause of flank pain. Osteomalacia of the ribs was infrequently encountered as the cause of flank pain.

Uric acid in the pathogenesis of metabolic, renal, and cardiovascular diseases: A review.

The association between uric acid (UA) on one side and systemic hypertension (Htn), dyslipidemia, glucose intolerance, overweight, fatty liver, renal disease and cardiovascular disease (CVD) on the other side is well recognized. However, the causal relationship between UA and these different clinical problems is still debatable. The recent years have witnessed hundreds of experimental and clinical trials that favored the opinion that UA is a probable player in the pathogenesis of these disease entities.

Diabetic nephropathy: Time to withhold development and progression - A review.

The recent discoveries in the fields of pathogenesis and management of diabetic nephropathy have revolutionized the knowledge about this disease. Little was added to the management of diabetic nephropathy after the introduction of renin angiotensin system blockers. The ineffective role of the renin- angiotensin system blockers in primary prevention of diabetic nephropathy in type 1 diabetes mellitus necessitated the search for other early therapeutic interventions that target alternative pathogenic mechanisms.

Is Fibroblast growth factor 23 the leading cause of increased mortality among chronic kidney disease patients? A narrative review.

The death rate among chronic kidney disease patients is the highest compared to other chronic diseases. 60% of these fatalities are cardiovascular. Cardiovascular calcifications and chronic inflammation affect almost all chronic kidney disease patients and are associated with cardiovascular mortality.

FGF23 and inflammation.

Systemic inflammation is a recognized feature in chronic kidney disease (CKD). The role of systemic inflammation in the pathogenesis of vascular calcification was recently settled. FGF23 was recently accused as a direct stimulus of systemic inflammation.

Vascular calcification: When should we interfere in chronic kidney disease patients and how?

Chronic kidney disease (CKD) patients are endangered with the highest mortality rate compared to other chronic diseases. Cardiovascular events account for up to 60% of the fatalities. Cardiovascular calcifications affect most of the CKD patients.

Stop chronic kidney disease progression: Time is approaching.

Progression of chronic kidney disease (CKD) is inevitable. However, the last decade has witnessed tremendous achievements in this field. Today we are optimistic; the dream of withholding this progression is about to be realistic.

The Association between Fibroblast Growth Factor-23 and Vascular Calcification Is Mitigated by Inflammation Markers.

Background: Fibroblast growth factor-23 (FGF-23) has been linked to vascular calcification, ventricular hypertrophy and mortality in chronic kidney disease (CKD), although these links may not be direct and independent. Similar grave outcomes are associated with inflammation and oxidative stress in CKD. Recently, accumulating evidence has linked components of phosphate homeostasis to inflammation and oxidative stress.

Endogenous soluble receptor of advanced glycation end-products (esRAGE) is negatively associated with vascular calcification in non-diabetic hemodialysis patients.

Background: Advanced glycation end-products (AGE) accumulate in CKD and may predispose to cardiovascular disease by inducing inflammatory and oxidant stress in the vascular endothelium. Soluble forms of the receptor for AGE (RAGE) may be protective against these effects by binding AGE in the soluble phase. Accumulating evidence suggests a protective role of soluble RAGE against vascular calcification.

Fibroblast growth factor-23 (FGF-23) is independently correlated to aortic calcification in haemodialysis patients.

Background: Vascular calcification has detrimental consequences on chronic kidney disease (CKD) patients, yet its pathogenesis is not fully understood. Fibroblast growth factor-23 (FGF-23) is involved in the regulation of mineral metabolism which may in turn affect vascular calcification. Data on the relationship between FGF-23 and peripheral vascular calcification, using conventional radiographs, are conflicting, and less is known about its relation to aortic calcification.