Exploring kidney biopsy findings in congenital heart diseases: Insights beyond cyanotic nephropathy.

BACKGROUND: The association between congenital heart disease and chronic kidney disease is well known. Various mechanisms of kidney damage associated with congenital heart disease have been established. The etiology of kidneydisease has commonly been considered to be secondary to focal segmental glomerulosclerosis (FSGS), however, this has only been demonstrated in case reports and not in observational or clinical trials. AIM: To identify baseline and clinical characteristics, as well as the findings in kidney biopsies of patients with congenital heart disease in our hospital. METHODS: This is a retrospective observational study conducted at the Nephrology Department of the National Institute of Cardiology "Ignacio Chávez". All patients over 16 years old who underwent percutaneous kidney biopsy from January 2000 to January 2023 with congenital heart disease were included in the study. RESULTS: Ten patients with congenital heart disease and kidney biopsy were found. The average age was 29.00 years ± 15.87 years with pre-biopsy proteinuria of 6193 mg/24 h ± 6165 mg/24 h. The most common congenital heart disease was Fallot's tetralogy with 2 cases (20%) and ventricular septal defect with 2 (20%) cases. Among the 10 cases, one case of IgA nephropathy and one case of membranoproliferative glomerulonephritis associated with immune complexes were found, receiving specific treatment after histopathological diagnosis, delaying the initiation of kidney replacement therapy. Among remaining 8 cases (80%), one case of FSGS with perihilar variety was found, while the other 7 cases were non-specific FSGS. CONCLUSION: Determining the cause of chronic kidney disease can help in delaying the need for kidney replacement therapy. In 2 out of 10 patients in our study, interventions were performed, and initiation of kidney replacement therapy was delayed. Prospective studies are needed to determine the usefulness of kidney biopsy in patients with congenital heart disease.

Classification of Acute Rejection Episodes in Kidney Transplantation: a Proposal Based on Factor Analysis.

INTRODUCTION: Kidney transplantation is considered the ideal treatment for end-stage renal disease. Acute rejection can influence graft survival. The aim of this study was to propose a classification system for acute rejection based on factor analysis. MATERIALS AND METHODS: Data were collected from kidney transplant recipients with acute rejection diagnosis based on standard histological variables, the presence of peritubular eosinophils, and immunolabeling for lysozyme and myeloperoxidase in kidney tissue. Factor analysis was employed for data reduction and generation of a new case classification, with orthogonal rotation as a strategy to simplify factors, and principal component analysis was used as an extraction method. RESULTS: Seventy-nine kidney biopsies were obtained from 74 patients. The total population was divided into humoral rejection (39.2%), cellular rejection (34.1%), and mixed acute rejection (26.7%). No significant differences were found between the three groups in clinical and biochemical variables. We extracted 4 factors using factor analysis. The 1st factor was characterized by the presence of capillaritis, plasma cells infiltration, tubulitis, and inflammation. The 2nd factor included positivity for lysozyme and myeloperoxidase, while the 3rd factor included the presence of eosinophils and glomerulitis. The 4th component consisted of the presence of C4d and endarteritis. The cases belonging to the 3rd factor showed the greatest increase in serum creatinine. The cases belonging to the 4th factor exhibited greater urinary excretion of proteins. CONCLUSIONS: This proposal of classification of acute rejection could contribute to evaluate the prognosis of kidney transplant recipients.

A pilot study on the impact of a low fructose diet and allopurinol on clinic blood pressure among overweight and prehypertensive subjects: a randomized placebo controlled trial.

Fructose and sodium intake have been associated with hypertension and metabolic syndrome. Although various mechanisms are involved, fructose causes hypertension partly through rising intracellular and serum uric acid. To date, there are no studies in adults that have evaluated the impact of low fructose diets and allopurinol on prehypertensive and overweight subjects. The objective of this study was to compare the effect of low fructose diet and allopurinol or placebo on blood pressure (BP) and metabolic syndrome components The study was a controlled clinical trial and consisted of two phases; in the first phase of intervention (4 weeks), patients were randomized to either low fructose diet (34 patients) or control diet (38 patients). In the second phase of intervention (weeks 4-8), the same groups continued with the same diet prescriptions but were further randomized to receive placebo or allopurinol (300 mg/d). Clinic and 24-hour ambulatory BP, anthropometric measures, and laboratory data were determined at baseline, weeks 4 and 8. Seventy-two patients were included in the trial. At the end of the dietary phase, both diet groups significantly reduced their BP, but there were no between-group differences. Compared to placebo, at the end of follow-up, subjects in the allopurinol group had a lower clinic systolic blood pressure and this was significant within- and between-group comparisons. The percentage of dippers was higher in the allopurinol group, and weight was reduced significantly despite the absence of caloric restriction Allopurinol was associated with a significant reduction in clinic BP, an increase in the percentage of dippers, and significant weight loss. Larger studies with longer follow-up are needed to confirm our findings.

Determinación del transporte peritoneal de fósforo como herramienta para el control del fósforo sérico / Determination of peritoneal phosphate transport as a tool for controlling serum phosphorus

Introducción: La hiperfosfatemia (fósforo sérico ≥ 5,5 mg/dl) es un factor independiente de mortalidad en la población en diálisis. Comparamos el transporte peritoneal de fósforo, creatinina y urea para demostrar diferencias y señalar la relevancia de estos parámetros en el control del fósforo sérico. Material y métodos: Se incluyeron 60 pacientes en diálisis peritoneal y se determinó el índice dializante/plasma de fósforo (D/P P) y creatinina (D/P Cr), el aclaramiento semanal de fósforo (AclP) y creatinina (AclCr), Kt/V de urea semanal y la excreción peritoneal de fósforo (ExP). Resultados: El D/P P fue superior en pacientes con normofosfatemia, comparados con los que presentaron hiperfosfatemia, 0,61 ± 0,13 frente a 0,54 ± 0,10 (p = 0,035). Se observó una adecuada correlación entre el D/P P y el D/P Cr, r = 0,90, p < 0,05, pero una pobre concordancia entre ambos, con un límite inferior de −0,17 (−0,24 a −0,09 IC 95 %) y límite superior de 0,47 (0,39-0,54 IC 95 %) para el D/P Cr respecto al D/P P. El AclP tuvo una adecuada correlación con el D/P P en pacientes con Kt/V ≥ 1,7 (r = 0,384, p = 0,04) y en anúricos (r = 0,392, p = 0,04), pero no con el D/P Cr. Hubo una pobre concordancia del AclCr respecto al AclP con límite inferior de -13,54 l/sem/1,73 m2 SC (-21,68 a -5,4 IC 95 %) y límite superior de 58,98 l/sem/1,73 m2 SC (50,84-67,12 IC 95 %). La ExP total se relacionó con el AclP (r = 0,643, p < 0,05), mientras que no lo hizo con el AclCr (r = 0,222, p = 0,23). Mediante el método CHAID se realizó un árbol de clasificación del transporte de fósforo con base en su D/P, obteniendo 5 nodos (≤ 0,5, 0,51-0,55, 0,56-0,66, 0,67-0,76, > 0,76), mostrando diferencias estadísticamente significativas entre nodos para niveles séricos de fósforo, AclP total y peritoneal, así como Kt/V de urea semanal. Conclusiones: Las mediciones de D/P P y AclP no concuerdan con las mediciones de D/P Cr y AclCr, respectivamente, por lo que su determinación es una herramienta clínica para el control del nivel de fósforo sérico (AU)

Background: Hyperphosphataemia (serum phosphorus ≥5.5mg/dl) is an independent mortality factor for the dialysis population. We compared phosphorus, creatinine and urea peritoneal transport to demonstrate differences and indicate the relevance of these parameters in the control of serum phosphorus. Material and method: We included 60 patients on peritoneal dialysis and determined the dialysate/plasma phosphorus (D/P P) and creatinine (D/P Cr) ratios, weekly creatinine clearance (CrCl) and phosphorus clearance (PCl), weekly Kt/V of urea, and peritoneal phosphorus excretion (PEx). Results: D/P P was higher in patients with normal phosphataemia, compared with those who were hyperphosphataemic 0.61±0.13 versus 0.54±0.10 (p=.035). We observed an adequate correlation between D/P P and D/P Cr, r=0.90, p<.05, but poor concordance between both, with a lower limit of -0.17 (-0.24 to -0.09 95% CI) and an upper limit of 0.47 (0.39-0.54 95% CI) for D/P Cr with respect to D/P P. PCl had an adequate correlation with D/P P in patients with a Kt/V ≥1.7 (r=0.384, p=.04) and in anuric patients (r=0.392, p=.04), but not with D/P Cr. There was poor concordance of the CrCl with respect to PCl with a lower limit of -13.54l/week/1.73m2 BSA (-21.68 to -5.4 95% CI) and an upper limit of 58.98l/week/1.73m2 BSA (50.84-67.12 95% CI). Total PEx was related to PCl (r=0.643, p<.05), while it was not related to CrCl (r=0.222, p=.23). Using the CHAID method, we created a classification tree for phosphorus transport based on its D/P, obtaining 5 nodes (≤0.5, 0.51-0.55, 0.56-0.66, 0.67-0.76, >0.76), with statistically significant differences between nodes for serum phosphorus, total and peritoneal PCl and weekly Kt/V of urea. Conclusions: D/P P and PCl are not concordant with D/P Cr and CrCl respectively and therefore their determination is a clinical tool to control serum phosphorus levels

Determination of peritoneal phosphate transport as a tool for controlling serum phosphorus.

BACKGROUND: Hyperphosphataemia (serum phosphorus ≥5.5mg/dl) is an independent mortality factor for the dialysis population. We compared phosphorus, creatinine and urea peritoneal transport to demonstrate differences and indicate the relevance of these parameters in the control of serum phosphorus. MATERIAL AND METHOD: We included 60 patients on peritoneal dialysis and determined the dialysate/plasma phosphorus (D/P P) and creatinine (D/P Cr) ratios, weekly creatinine clearance (CrCl) and phosphorus clearance (PCl), weekly Kt/V of urea, and peritoneal phosphorus excretion (PEx). RESULTS: D/P P was higher in patients with normal phosphataemia, compared with those who were hyperphosphataemic 0.61±0.13 versus 0.54±0.10 (p=.035). We observed an adequate correlation between D/P P and D/P Cr, r=0.90, p<.05, but poor concordance between both, with a lower limit of −0.17 (−0.24 to −0.09 95% CI) and an upper limit of 0.47 (0.39-0.54 95% CI) for D/P Cr with respect to D/P P. PCl had an adequate correlation with D/P P in patients with a Kt/V ≥1.7 (r=0.384, p=.04) and in anuric patients (r=0.392, p=.04), but not with D/P Cr. There was poor concordance of the CrCl with respect to PCl with a lower limit of −13.54l/week/1.73m2 BSA (−21.68 to −5.4 95% CI) and an upper limit of 58.98l/week/1.73m2 BSA (50.84-67.12 95% CI). Total PEx was related to PCl (r=0.643, p<.05), while it was not related to CrCl (r=0.222, p=.23). Using the CHAID method, we created a classification tree for phosphorus transport based on its D/P, obtaining 5 nodes (≤0.5, 0.51-0.55, 0.56-0.66, 0.67-0.76, >0.76), with statistically significant differences between nodes for serum phosphorus, total and peritoneal PCl and weekly Kt/V of urea. CONCLUSIONS: D/P P and PCl are not concordant with D/P Cr and CrCl respectively and therefore their determination is a clinical tool to control serum phosphorus levels.

Aldosterone synthase gene polymorphism and renal histopathologic changes in kidney transplant patients receiving a calcineurin inhibitor.

INTRODUCTION: Aldosterone participates in the pathogenesis of calcineurin inhibitor nephrotoxicity (CIN), producing renal vasoconstriction and transforming growth factor beta (TGFß) expression. The objective of this study was to assess aldosterone polymorphisms and relationships to plasma aldosterone levels and the development of renal histological lesions in kidney transplant patients. MATERIAL AND METHODS: Patients with kidney graft biopsy were divided according to the presence or absence of CIN. We determined aldosterone synthase (AS) -344 T/C and int 2 W/C gene polymorphisms and plasma aldosterone levels. Histological, biochemical and clinical variables were measured. RESULTS: Calcineurin inhibitor (CI) levels were significantly higher in patients with the int 2 WW genotype than in patients with WC or CC genotypes. There was a greater degree of interstitial fibrosis in patients with int 2 CC genotype. No relationship was found between the different polymorphisms and a higher degree and/or frequency of CIN. There was also no relationship with plasma aldosterone levels. CONCLUSION: The frequency of the different polymorphisms studied was not related to plasma aldosterone levels or the development of CIN; however, the int 2 CC genotype was related to a greater degree of interstitial fibrosis, whereas the WW genotype was related to higher CI serum levels.

Nefrocalcinosis y acidosis tubular renal distal en síndrome de Sjögren / Nephrocalcinosis and distal renal tubular acidosis in Sjögren's syndrome

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Asociación entre excreción peritoneal de proteínas, episodios de peritonitis y D/P de fósforo en pacientes en diálisis peritoneal / Association between peritoneal protein excretion, peritonitis and D/P phosphate, in patients on peritoneal dialysis

Introducción: Se ha observado una relación entre el aumento de la transferencia de solutos (aumento del D/P de creatinina) y la disminución de la ultrafiltración, el aumento de la mortalidad y el riesgo de fracaso de la técnica en pacientes en diálisis peritoneal (DP). Las altas tasas de transporte de solutos se asocian con una mayor excreción peritoneal de proteínas (EPP) y esto se ha relacionado con un mayor riesgo de peritonitis. Nuestro objetivo fue evaluar la posible asociación entre la EPP, el número de episodios de peritonitis y el D/P de fósforo. Material y métodos: Se realizó un estudió longitudinal de cohorte prospectivo en pacientes en DP, a los que se les midió el D/P de fósforo, la EPP, el número de episodios de peritonitis, parámetros de adecuación, así como diferentes variables clínicas y bioquímicas. Resultados: Se incluyeron 60 pacientes en programa de DP ambulatoria. Se encontró una correlación significativa positiva (r = 0,369; p = 0,005) entre el D/P de fósforo y la EPP, al igual que entre la EPP y el número de episodios de peritonitis (r = 0,65; p = 0,044). Finalmente, se encontró que a mayor EPP y a mayor D/P de fósforo, menor nivel sérico de albumina (r = -0,50, p = 0,001 y r = -0,621, p = 0,000, respectivamente). Conclusiones: La EPP se asocia significativamente con el número de episodios de peritonitis y el D/P de fósforo (AU)

Introduction: There is a relationship between increased transfer of solutes (increased D/P creatinine) and decreased ultrafiltration, increased mortality and risk of technique failure in peritoneal dialysis patients. High rates of solute transport are associated with increased peritoneal protein excretion (PPE) and this has been associated with an increased risk of peritonitis. Our objective was to evaluate the possible association between the PPE, the number of episodes of peritonitis and the D/P phosphate. Material and methods: A prospective longitudinal cohort study in PD patients. D/P phosphate, PPE, the number of episodes of peritonitis, as well as adequacy parameters and clinical and biochemical variables were measured. Results: We included 60 patients on ambulatory peritoneal dialysis. We found a significant positive correlation (r=.369, P=.005) between the D/P phosphate and PPE, as well as between the PPE and the number of episodes of peritonitis (r=.65, p=.044). Finally, we found that the higher PPE and D/P phosphate, the lower serum albumin was (r=-0.50, p=.001 and r=-0.621, p=.000, respectively). Conclusions: The EPP is significantly associated with the number of episodes of peritonitis and the D/P phosphate (AU)

Association between peritoneal protein excretion, peritonitis and D/P phosphate, in patients on peritoneal dialysis.

INTRODUCTION: There is a relationship between increased transfer of solutes (increased D/P creatinine) and decreased ultrafiltration, increased mortality and risk of technique failure in peritoneal dialysis patients. High rates of solute transport are associated with increased peritoneal protein excretion (PPE) and this has been associated with an increased risk of peritonitis. Our objective was to evaluate the possible association between the PPE, the number of episodes of peritonitis and the D/P phosphate. MATERIAL AND METHODS: A prospective longitudinal cohort study in PD patients. D/P phosphate, PPE, the number of episodes of peritonitis, as well as adequacy parameters and clinical and biochemical variables were measured. RESULTS: We included 60 patients on ambulatory peritoneal dialysis. We found a significant positive correlation (r=.369, P=.005) between the D/P phosphate and PPE, as well as between the PPE and the number of episodes of peritonitis (r=.65, p=.044). Finally, we found that the higher PPE and D/P phosphate, the lower serum albumin was (r=­0.50, p=.001 and r=­0.621, p=.000, respectively). CONCLUSIONS: PPE is significantly associated with the number of episodes of peritonitis and the D/P phosphate.

[Salt-sensitive hypertension]. / Hipertensión arterial sistémica y sensibilidad a la sal.

Individuals with elevated blood pressure are at increased risk for cardiovascular events and death. Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age. Salt sensitivity has been linked to an increased risk for the development of left ventricular hypertrophy, proteinuria, and a blunted nocturnal decline in blood pressure ("non-dipping"). Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or "pressure natriuresis". The development of salt-sensitive hypertension is proposed to occur in three phases. In the first phase, the kidney is structurally normal, and sodium is excreted normally. However, the kidney may be exposed to various stimuli that result in renal vasoconstriction. In the second phase, subtle renal injury develops, impairing sodium excretion and leading to an increase in blood pressure. In the third phase, the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium handling. Other mechanisms, such as primary tubulointerstitial disease, genetic alterations in sodium regulation and excretion, or a congenital reduction in nephron number that limits sodium filtration are important in the development of salt-sensitive hypertension.

Hipertensión arterial sistémica y sensibilidad a la sal / Salt-sensitive hypertension

Individuals with elevated blood pressure are at increased risk for cardiovascular events and death. Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age. Salt sensitivity has been linked to an increased risk for the development of left ventricular hypertrophy, proteinuria, and a blunted nocturnal decline in blood pressure ([quot ]non-dipping[quot ]). Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or [quot ]pressure natriuresis[quot ]. The development of salt-sensitive hypertension is proposed to occur in three phases. In the first phase, the kidney is structurally normal, and sodium is excreted normally. However, the kidney may be exposed to various stimuli that result in renal vasoconstriction. In the second phase, subtle renal injury develops, impairing sodium excretion and leading to an increase in blood pressure. In the third phase, the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium handling. Other mechanisms, such as primary tubulointerstitial disease, genetic alterations in sodium regulation and excretion, or a congenital reduction in nephron number that limits sodium filtration are important in the development of salt-sensitive hypertension.