<b><i>Introduction:</i></b> Peritoneal protein loss (PPL) has been associated with mortality. Inflammation was assumed a putative cause with malnutrition as a consequence. Hydrostatic convection is a major drive for microvascular protein transport, but most studies in peritoneal dialysis (PD) patients overlooked this mechanism. An association between peritoneal protein clearance (PPCl) and venous congestion has been reported recently. The aim of this study was to explore the importance of fluid overload in PPCl in PD. <b><i>Methods:</i></b> Sixty-seven prevalent PD patients were assessed with peritoneal equilibration test and multifrequency bioelectrical impedance assessment (BIA). PPL and PPCl were calculated from simultaneously obtained 24-h peritoneal effluent. <b><i>Results:</i></b> PPL averaged 5.2 g/24 h. It was higher in patients on continuous treatment than in those without a long dwell. Significant associations between PPCl and BIA parameters of overhydration were found in both univariable and multivariable analyses. Lean mass index, partly dependent on hydration status, was associated with PPCl in univariable but not in multivariable analysis. A multiple linear model identified extracellular water excess and higher D/P creatinine as predictors of higher PPCl, independent of PD duration, type of PD, age, gender, albumin, cardiovascular disease, C-reactive protein, or lean mass index. <b><i>Conclusions:</i></b> The uni- and multivariable strong associations between fluid overload and PPCl support the importance of hydrostatic pressure-induced convection for PPCl. Also, peritoneal small solute transport was associated with PPCl. Both are amenable by adjusted dialysis prescription, especially focused on fluid status and avoidance of overhydration. The assumption of an association with inflammation and malnutrition was not confirmed.

Peritoneal protein loss (PPL) has been correlated with mortality, malnutrition and inflammation. More recently overhydration was brought to the equation. This study aims to review classic and recent factors associated with PPL. Prevalent and incident peritoneal dialysis (PD) patients were included. Dialysate and serum IL-6 was obtained during PET. Hydration and nutritional status were assessed by bio-impedance. Linear regression and Cox regression were performed. The 78 included patients presented median values of PPL 4.8 g/24 h, serum IL-6: 5.1 pg/mL, and IL-6 appearance rate 153.5 pg/min. Mean extracellular water excess (EWexc) was 0.88 ± 0.94 L, and lean body mass index (LBMI) 17.3 ± 2.4 kg/m2. After mean follow-up of 33.9 ± 29.3 months, 12 patients died. Linear univariable analysis showed positive associations between PPL and small solute transport, body composition (LBMI and EWexc), comorbidities and performing CAPD (vs. cycler). PPL correlated positively with dialysate appearance rate of IL-6, but not with serum IL-6. Linear multivariable analysis confirmed positive association between PPL and EWexc (p = 0.012; 95%CI: 4.162–31.854), LBMI (p = 0.008; 95%CI: 1.720–11.219) and performing CAPD (p = 0.023; 95%CI: 4.375–54.190). In survival analysis, no relationship was found between mortality and PPL. Multivariable Cox regression showed Charlson Comorbidity Index (HR: 1.896, 95%CI: 1.235–2.913), overhydration (HR: 10.034, 95%CI: 1.426–70.587) and lower PPL (HR: 0.576, 95%CI: 0.339–0.978) were predictors for mortality. Overhydration, was a strong predictor of PPL, overpowering variables previously reported as determinants of PPL, namely clinical correlates of endothelial dysfunction or local inflammation. PPL were not associated with malnutrition or higher mortality, emphasizing the importance of volume overload control in PD patients.

<b><i>Introduction:</i></b> Quantification of peritoneal protein loss (PPL) may be expressed according to a timely collection (24-h measurement or 4-h PET assessment) and as a concentration. The aim of this study was to compare the quantification methods of 24-h and 4-h collections. <b><i>Methods:</i></b> This study included 81 prevalent peritoneal dialysis patients. Demographics and clinical and bioelectrical impedance features were registered. PPL was measured (4-h PET and 24-h results) and peritoneal protein clearance was calculated. A linear regression model was performed. <b><i>Results:</i></b> Age and continuous ambulatory peritoneal dialysis (compared to cycler) were positively associated with greater PPL on 24-h collections. Neither cardiovascular disease, hypertension, diabetes nor the comorbidity Charlson Index was significantly associated with PPL. There was a consistent univariable relationship with D/P creatinine, whichever sampling method was used. Only 24-h measurements of PPL correlated with body composition variables. In multiple linear regression analysis, D/P creatinine association with PPL stands out. On the other hand, 24-h determinations (in grams or clearance) were associated with overhydration. PET protein quantification was associated with peritoneal creatinine clearance. <b><i>Discussion/Conclusion:</i></b> Different methods sign different pathophysiological pathways. PET protein loss quantification should be regarded as a marker of peritoneal membrane intrinsic permeability. Measurements of a 24-h sample might be closer to patients’ clinical status and prognosis, signalizing opportunities for therapy intervention.

Acute kidney injury is a common complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Several pathologic findings are continually being reported, showing a probably multifactorial etiology. The authors present a case of a patient diagnosed with a tip lesion variant of focal segmental glomerulosclerosis (FSGS) in the setting of COVID-19. A 43-year-old African American female with no known renal disease presented to the emergency department with a 6-day history of fatigue, headache, hypoageusia, myalgia, cough, nausea, and vomiting. Laboratory tests confirmed SARS-CoV-2 infection. During hospitalization, there was a progressive decline in kidney function and evidence of nephrotic-range proteinuria without nephrotic syndrome. Biopsy specimen showed a tip lesion variant of FSGS. Genetic test revealed a homozygous variant of uncertain clinical significance (c.397G&#x3e;A [p.V133M]) in the <i>epithelial membrane protein 2</i> (<i>EMP2</i>) gene. To our knowledge, this is the first case report of a tip lesion in a COVID-19 patient with no renal history. More studies are warranted to define susceptible groups and identify the detailed mechanisms of COVID-19-related kidney disease that would allow for specific management of this complication.

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A case of bilateral thrombosis of the renal arteries following blunt trauma is presented. The patient was a 12-year-old boy who was treated by chronic hemodialysis and subsequently renal transplantation. A review of the literature reveals only 8 such cases reported previously. The condition is unusual and requires early diagnosis because the success of renal vascularization is entirely dependent upon prompt timing of the operation.

BACKGROUND AND AIMS Recently, a growing number of studies have reported a close relationship between high serum calcium and low serum magnesium with vascular calcification. Endothelial dysfunction and vascular inflammation seem plausible risk factors for enhanced progression of kidney disease nevertheless, the knowledge remains scarce. The aim of this study is to evaluate the role of the calcium/magnesium ratio as a risk factor in CKD progression. METHOD Observational, prospective study involving 693 patients (f = 371, m = 322) with stage 4 and 5 CKD. Patients were divided into two groups, according to the development of end-stage renal disease (ESRD): G1 (n = 541), who did not undergo renal replacement therapy and G2 (n = 152), who had started renal replacement therapy (RRT). Several laboratory parameters were measured: haemoglobin, eGFR (MDRD), albumin, cholesterol, magnesium and mineral metabolism markers (PTH, calcium and phosphorus). Baseline characteristics were analysed and compared using Student%u2019s T-test for continuous variables and chi-squared test for categorical variables. Multivariate Cox regression analysis was used to identify independent factors associated with RRT initiation. A modified Poisson regression with robust error variance was used to estimate the cumulative relative risk for RRT initiation. RESULTS The mean age and estimated glomerular filtration rate (eGFR) of the study population was 70.09 ± 12.51 years and 19.91 ± 8.11 mL/min, respectively. Comparing the two groups, G2 had a significantly lower serum levels of Hb (11.75 versus 10.95 g/dL, P = 0.000), calcium (9.34 versus 8.95 mg/dL, P = 0.000), magnesium (1.92 versus 1.40 mg/dL, P = 0.0001), albumin (4.00 versus 3.88 g/dL, P = 0.03) and cholesterol (183.17 versus 172.39 mg/dL, P = 0.01) and a higher serum levels of phosphorus (3.88 versus 4.69 mg/dL, P = 0.0001), calcium/magnesium ratio (5.73 versus 7.56, P = 0.0001) and PTH (209.71 versus 338.84 pg/mL, P = 0.0001). In univariate Cox regression analysis, age, haemoglobin, eGFR, calcium, magnesium, phosphorus, calcium-magnesium ratio and PTH correlate with onset of RRT, which were further tested using a multivariate COX regression model. The results showed a clear relationship between high levels of phosphorus (HRa = 1.638, P = 0.001) and calcium-magnesium ratio (HRa = 1.292; P = 0.002), and low levels of magnesium (HRa = 0.761, P = 0.005) and eGFR (HRa = 0.934; P = 0.0001) were independent risk factors to start depurative techniques. Additionally, Poisson regression analysis showed that high calcium-magnesium ratios (aPR = 1.986; 95% CI 1.026–3.051; P = 0.002), high phosphorus levels (aPR = 1.607; 95% CI 1.324–1.950; P &lt; 0.0001) and low levels eGFR (aPR = 0.927; 95% CI 0.891–0.964; P &lt; 0.0001) were associated with a cumulative risk for initiation of RRT. CONCLUSION Our results suggest that the calcium/magnesium ratio is an independent predictive factor for the initiation of renal replacement therapy. Further studies are required to validate the use of this novel marker as a predictor of CKD progression.

Cardiovascular disease is the primary cause of morbidity and mortality in chronic kidney disease (CKD) population, particularly in end stage renal disease (ESRD). This could be explained in part due to the presence of traditional cardiovascular risk factors, such as older age, hypertension, dyslipidemia and diabetes, but is also associated with nontraditional cardiovascular risk factors related to CKD, like inflammation, anemia, abnormal calcium and phosphate metabolism and extracellular fluid volume overload, which may contribute to intimal or medial wall arterial calcification. Vascular calcification (VC) is a dynamic process, resulting from the dysregulation of the balance of molecules that promote and those that inhibit this course. It is important for clinicians to both acknowledge and recognize the pathways and risk factors of VC in order to improve cardiovascular health in CKD patients. This chapter will focus on the biology of VC, the association with CKD, risk factor modification, screening and prevention of VC and cardiovascular disease in CKD patients.