Diagnosis and treatment of type 2 diabetes mellitus in patients with chronic kidney disease and eGFR < 60 mL/min — a position statement of the Polish Society of Nephrology Working Group on Metabolic and Endocrine Disorders in Kidney Diseases

Diabetes mellitus is one the most frequent co-morbid conditions in patients with chronic kidney disease (CKD), frequently leading to chronic kidney failure. Progression of CKD accelerates several metabolic disorders, predominantly those related to abnormalities of carbohydrate metabolism. Patients with CKD are usually characterised by an insulin resistance additionally aggravated by several co-morbid conditions (for example chronic low-grade inflammation). Treatment with anti-diabetic medications in patients with CKD remains a challenge because, along with the disease progression, the dosing of several drugs needs to be adjusted to the reduced kidney function (especially those that are excreted intact with urine or as active metabolites). Progression of CKD also increases the risk of hypoglycaemia in patients treated with anti-diabetic drugs, and other adverse drug reactions may occur more frequently. Usefulness of the new generation drugs has not yet been verified in patients with advanced kidney disease (although some of them act through kidney-related mechanisms). The current position statement of the Polish Society of Nephrology Working Group provides practical recommendations for the diagnosis and treatment of type 2 diabetes mellitus in patients with CKD and reduced kidney function

Rozpoznawanie i leczenie cukrzycy typu 2 u chorych z przewlekłą chorobą nerek i wartością eGFR < 60 ml/min — opinia członków Grupy Roboczej Polskiego Towarzystwa Nefrologicznego ds. Zaburzeń Metabolicznych i Hormonalnych w Chorobach Nerek

Diabetes mellitus remains the most frequent co-morbid conditions in patients with chronic kidney disease (CKD) frequently leading to chronic kidney failure. Progression of CKD triggers several meta-bolic disorders, including those related to carbohy­drate metabolism. Patients with CKD are character­ized by an insulin resistance, additionally aggravated by several co-morbid conditions (such as for exam-ple chronic low-grade inflammation). Treatment with anti-diabetic medications in patients with CKD remains a challenge, since along with the progres­sion of a disease dosing of several drugs needs to be adjusted (especially of those which are excreted with urine intact or as active metabolites). CKD pro­gression also increases the risk of hypoglycemia in patients treated with anti-diabetic drugs and other adverse drug reactions. Usefulness of the new gen­eration drugs has not yet been verified in patients with advanced kidney disease (although some of them act through the kidney-related mechanisms). The current position statement of the Polish Society of Nephrology Working Group provides the practical guidelines for the diagnosis and treatment of type 2 diabetes mellitus in patients with CKD

Chronic opioid analgesic usage post‐kidney transplantation and clinical outcomes

Chronic opioid usage ( COU ) is common among patients with end‐stage renal disease ( ESRD ) qualified for kidney transplantation and associated with inferior post‐transplant outcomes. The magnitude of COU after kidney transplantation and its impact on transplant outcomes remain unknown. We performed a single‐center retrospective study aimed to describe the prevalence of COU during the first year, to identify the predictors of COU and to determine the impact of COU on post‐transplant outcomes including the rates of hospitalization and acute rejection during the first year, as well as long‐term patient and graft survival. Among 1045 kidney transplant patients, 119 (11.4%) had required continued outpatient prescription of opioid analgesics during the first year after kidney transplantation, mostly for non‐surgery‐related pain (85%). A positive history of COU prior to transplantation was the strongest predictor of COU in the first year post‐transplantation (adjusted odds ratio [ AOR ] 4.31, p < 0.001). Patients with COU had more often hospital admission during the first year ( AOR 2.48, p = 0.001, for 1 or 2 admissions, and AOR 6.03, p < 0.001 for ≥3 admissions), but similar rate of acute rejection (19.3% vs. 15.7%, p = 0.31). During long‐term follow‐up, however, the patient and/or death‐censored kidney survival was not different. COU early post‐kidney transplantation, when clinically indicated and properly supervised, does not appear to affect the risk of death and death‐censored graft failure.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/108587/1/ctr12414.pd

Effect of atorvastatin on iron metabolism regulation in patients with chronic kidney disease – a randomized double blind crossover study

Introduction: To determine the effect of 6-month administration of atorvastatin on hepcidin and hemojuvelin levels, inflammatory parameters and iron metabolism in patients with chronic kidney disease (CKD) stages 3 and 4. Methods: Thirty six statin- and erythropoiesis-stimulating agent-naive patients with CKD stages 3 and 4 and LDL cholesterol ≥100 mg/dl received atorvastatin or placebo for two 6-month periods in a double blind, randomized crossover study. Hepcidin, hemojuvelin, hsCRP, IL-6, hemoglobin, red blood cell distribution width, iron, total iron binding capacity (TIBC), and unsaturated iron binding capacity (UIBC) were measured before and after each treatment period. Results: Hepcidin decreased (from 102 [307] to 63 [170] pg/ml (p > .001)) in the course of statin therapy but remained unchanged after placebo administration (173 [256] to 153 [204] pg/ml, respectively). Hemojuvelin did not change after either part of the study. Both IL-6 and hsCRP decreased following statin therapy (from 8.7 [12.0] to 8.1 [13.9] pg/ml; p = .04 and from 4.7 [4.0] to 4.0 [3.6] mg/l; p = .4, respectively), but did not change after placebo administration. Blood hemoglobin increased slightly but significantly after 6-month statin therapy (from 11.6 ± 1.6 to 11.9 ± 1.5 g/dl, p = .002), and was unchanged after placebo treatment. TIBC and UIBC increased significantly after 6-month statin therapy, and serum iron also tended to increase. The change of eGFR during the study did not differ between the two treatment periods. Conclusions: Statin may have a small but potentially beneficial effect on serum hepcidin, which may lead to improvement of anemia control in CKD patients

Diagnosis and Treatment of Metabolic Acidosis in Patients with Chronic Kidney Disease – Position Statement of the Working Group of the Polish Society of Nephrology

Metabolic acidosis is commonly found in patients with chronic kidney disease (CKD), and its causes are: impaired ammonia excretion, reduced tubular bicarbonate reabsorption and insufficient renal bicarbonate production in relation to the amount of acids synthesised by the body and ingested with food. As the consequence, numerous metabolic abnormalities develop, which may lead to dysfunction of several organs. In observational studies, it has been found that CKD patients with metabolic acidosis are characterised by faster progression of kidney disease towards end stage kidney failure, and by increased mortality. Results of interventional studies suggest that alkali therapy in CKD patients slows progression of kidney disease. In view of these facts, the members of “The Working Group of the Polish Society of Nephrology on Metabolic and Endocrine Abnormalities in Kidney Diseases” have prepared the following statement and guidelines for the diagnosis and treatment of metabolic acidosis in CKD patients. Measurement of bicarbonate concentration in venous plasma or venous blood to check for metabolic acidosis should be performed in all CKD patients and metabolic acidosis in these patients should be diagnosed when the venous plasma or venous blood bicarbonate concentration is lower than 22 mmol/l. In patients with metabolic acidosis and CKD, oral sodium bicarbonate administration is recommended. The goal of such a treatment is to achieve a plasma or blood bicarbonate concentration equal to or greater than 22 mmol/l

Plasma Desphospho-Uncarboxylated Matrix Gla Protein as a Marker of Kidney Damage and Cardiovascular Risk in Advanced Stage of Chronic Kidney Disease

Background/Aims: Desphospho-uncarboxylated matrix Gla protein (dp-ucMGP) is formed as a result of vitamin K insufficiency. The aim of this study was to investigate the association between plasma dp-ucMGP, kidney function and cardiovascular risk factors before and after 9-months substitution of vitamin K2 in non-dialysis patients with chronic kidney disease (CKD) stage 4 and 5. Methods: 38 CKD patients were supplemented for 270±12 days with 90 µg vitamin K2 and 10 µg cholecalciferol or 10 µg cholecalciferol alone. At baseline and at follow-up circulating calcium, phosphate, lipids, hemoglobin, albumin and total protein, dp-ucMGP, osteoprotegerin, fetuin A, osteocalcin and fibroblast grown factor 23 (FGF-23) were assessed. Proteinuria was assessed in the first morning void. Results: Baseline plasma dp-ucMGP was 1018.6±498.3 pmol/l and was significantly higher in patients at stage 5 CKD (1388.3 ±505.4 pmol/l) than at stage 4 (885.1±419.7 pmol/l), p=0.04. Vitamin K2 supplementation resulted in a decrease of dp-ucMGP level by 10.7%. Plasma dp-ucMGP was positively associated with proteinuria, serum creatinine, PTH and FGF-23; and inversely associated with glomerular filtration rate, serum hemoglobin and albumin. Conclusions: High dp-ucMGP level, reflecting a poor vitamin K status seems to be associated with kidney damage and may be also a marker of cardiovascular risk in CKD patients. Supplementation with vitamin K2 may improve the carboxylation status of MGP