Rafael Selgas

Thyroid dysfunction and kidney disease: An update

Thyroid hormones influence renal development, kidney hemodynamics, glomerular filtration rate and sodium and water homeostasis. Hypothyroidism and hyperthyroidism affect renal function by direct renal effects as well as systemic hemodynamic, metabolic and cardiovascular effects. Hypothyroidism has been associated with increased serum creatinine and decreased glomerular filtration rate. The reverse effects have been reported in thyrotoxicosis. Most of renal manifestations of thyroid dysfunction are reversible with treatment. Kidney disease may also cause thyroid dysfunction by several mechanisms. Nephrotic syndrome has been associated to changes in serum thyroid hormone concentrations. Different forms of glomerulonephritis and tubulointerstitial disease may be linked to thyroid derangements. A high prevalence of thyroid hormone alteration has been reported in acute kidney injury. Thyroid dysfunction is highly prevalent in chronic kidney disease patients. Subclinical hypothyroidism and low triiodothyronine syndrome are common features in patients with chronic kidney disease. Patients treated by both hemodialysis and peritoneal dialysis, and renal transplantation recipients, exhibit thyroid hormone alterations and thyroid disease with higher frequency than that found in the general population. Drugs used in the therapy of thyroid disease may lead to renal complications and, similarly, drugs used in kidney disorders may be associated to thyroid alterations. Lastly, low thyroid hormones, especially low triiodothyronine levels, in patients with chronic kidney disease have been related to a higher risk of cardiovascular disease and all-cause mortality. Interpretation of the interactions between thyroid and renal function is a challenge for clinicians involved in the treatment of patients with thyroid and kidney disease.

The Communication and Bioethical Training (CoBiT) Program for assisting dialysis decision-making in Spanish ACKD units

Abstract Healthcare professionals currently working in Advanced Chronic Kidney Disease (ACKD) units must cope with difficult situations regarding assisting patients with the dialysis decision-making process, and they are often untrained for these conversations. Although we have evidence from the literature that these skills can be learned, few professionals feel confident in this area. A Communication and Bioethical Training (CoBiT) Program for ACKD staff (physicians, nurses and allied health professionals) was developed to improve their ability and self-confidence in conducting these conversations. A four-stage study was conducted: (1) development of the CoBiT program, beginning with the creation of an interdisciplinary focus group (N = 10); (2) design of a questionnaire to assess self-confidence based on the areas identified by the focus group. The face validity of the instrument was tested using an inter-judge methodology (N = 6); (3) design of the format and contents of the program; (4) piloting the program. Thirty-six health professionals took an 8-h workshop based on role-playing methodology. Participants assessed their self-confidence in their communication skills before and after the program using self-report measures. The results show that after the program, participants reported significantly higher levels of self-confidence measured with a five-point Likert scale (p < 0.001). Participants felt that communication with colleagues of other professions significantly increased after the workshop (p = 0.004). The CoBiT program improves ACKD Unit healthcare professionals’ self-confidence in their ability to perform a specific communication task.

Occult Hepatitis C Virus Infection in Patients with Diabetic Nephropathy: Epidemiological and Clinical Implications

Background:A high prevalence of hepatitis C virus (HCV) infection in patients with diabetic kidney disease (DKD) has been reported. However, the epidemiology and relationship between DKD and occult HCV infection (OCI)are unknown.Objetives: To determine the prevalence of OCI in a population without conventional markers of HCV infection diagnosed with DKD, and to study its possible clinical implications.Study design: This prospective study included 125 anti-HCV and serum HCV-RNA-negative patients with DKD for the presence of OCI. HCV-RNA was tested by real-time reverse transcription PCR in peripheral blood mononuclear cells and in plasma after ultracentrifugation. Results: OCI was positive in 10 patients (8%). The patients with OCI had significantly higher ferritin levels (p=.002) and monoclonal gammopathy (30% [3/10] vs. 0.87% [1/115] than the patients without OCI [p=.003]). We found similar plasma ALT and GGT levels and HbA1C in both groups. At the end of the follow-up, the progression rate of renal disease tended to be faster in the group with OCI relative to the negative one, but without a significant difference. We did not find an association between OCI and cardiovascular morbidity. Conclusions: There was an 8% prevalence of OCI in patients with chronic renal failure secondary to DKD, higher than in the general population. This occult infection does not appear to play a role in the control of diabetes, cardiovascular risk or steatosis. However, the progression rate of renal disease tended to be faster, and the incidence of associated monoclonal gammopathy was significant.

Pharmacological Preservation of Peritoneal Membrane in Peritoneal Dialysis

Peritoneal dialysis (PD) is an established renal replacement therapy for renal disease. It is based on the capacity of the peritoneum to act as a semipermeable membrane for the exchange of toxic solutes and water, which is called ultrafiltration capacity. Peritoneal membrane (PM) is lined by a monolayer of mesothelial cells (MCs), which lay on an extracellular matrix bed where other cell types and blood and lymphatic vessels can be found. Long-term exposure to hyperosmotic PD fluids (PDFs), peritonitis or hemoperitoneum causes peritoneal injury by the generation of an inflammatory state. Inflammatory cells and their mediators initiate a cascade of reactions promoting alterations in peritoneal cells, loss of MCs, fibrosis, vasculopathy, and angiogenesis, leading to ultrafiltration failure. Recent studies support that the so-called “mesothelial to mesenchymal transition” process of the MCs runs parallel to the anatomical and functional ridging of PM, which suggests that its inhibition might slow down or stop the PM damage. The fight against PM damage begins with the improvement in PDF biocompatibility. Complementary to this, an alternative approach to preserve the PM might be the use of pharmacological agents or molecular strategies. Here, we explain the existing research models for the development of new therapies and analyze several therapeutic options tested with them.