Hypercalcemia as an Early Finding of Opportunistic Fungal Pneumonia in Renal Transplantation: A Case Series Report.

BACKGROUND: Pneumonia caused by opportunistic fungi is a serious complication in immunocompromised patients. Hypercalcemia has been described in renal transplantation associated with Pneumocystis jirovecii (PJP) or Histoplasma capsulatum (HCP) pneumonia. METHODS: We describe 5 patients who underwent kidney transplant between 2014 and 2019 and developed hypercalcemia before the diagnosis of pulmonary fungal infection: 4 patients with PJP and 1 with HCP. We assessed calcium metabolism and kidney function by total and ionized calcium, phosphorus, intact parathormone (iPTH), 25-OH vitamin D, 1,25(OH)2 vitamin D, and serum creatinine levels. RESULTS: Mean albumin-corrected calcium and ionized calcium were 12.56 mg/dL (range, 10.8-13.8 mg/dL) and 1.57 mmol/L (range, 1.43-1.69 mmol/L). Patients were normocalcemic, at 10.12 mg/dL (range, 9.6-10.5 mg/dL), before diagnosis and resolved hypercalcemia after antifungal treatment, at 8.86 mg/dL (range, 8.0-9.5 mg/dL). All patients had low or normal iPTH values, at 29.1 pg/mL (range, <3-44 pg/mL), with higher PTH levels 3 months before diagnosis and after treatment, at 147.3 pg/mL (range, 28.1-479 pg/mL) and 117.5 pg/mL (range, 18.2-245 pg/mL), respectively. The mean value for 25-OH vitamin D was 30.8 ng/mL (range, 14.6-62.8 ng/mL). This supports a PTH-independent mechanism, and we postulated an extrarenal production of 1,25(OH)2 vitamin D. CONCLUSION: In kidney transplant patients, hypercalcemia independent of PTH and refractory to treatment should alert for the possibility of opportunistic fungal pneumonia.

Hyponatremia in kidney transplant patients: its pathophysiologic mechanisms.

Kidney transplant patients (KTPs), and particularly those with advanced chronic kidney rejection, may be affected by opportunistic infections, metabolic alterations and vascular and oncologic diseases that promote clinical conditions that require a variety of treatments, the combinations of which may predispose them to hyponatremia. Salt and water imbalance can induce abnormalities in volemia and/or serum sodium depending on the nature of this alteration (increase or decrease), its absolute magnitude (mild or severe) and its relative magnitude (body sodium:water ratio). Hyponatremia appears when the body sodium:water ratio is reduced due to an increase in body water or a reduction in body sodium. Additionally, hyponatremia is classified as normotonic, hypertonic and hypotonic and while hypotonic hyponatremia is classified in hyponatremia with normal, high or low extracellular fluid. The main causes of hyponatremia in KTPs are hypotonic hyponatremia secondary to water and salt contraction with oral hydration (gastroenteritis, sepsis), free water retention (severe renal failure, syndrome of inappropriate antidiuretic hormone release, hypothyroidism), chronic hypokalemia (rapamycin, malnutrition), sodium loss (tubular dysfunction secondary to nephrocalcinosis, acute tubular necrosis, tubulitis/rejection, interstitial nephritis, adrenal insufficiency, aldosterone resistance, pancreatic drainage, kidney-pancreas transplant) and hyponatremia induced by medication (opioids, cyclophosphamide, psychoactive, potent diuretics and calcineurinic inhibitors). In conclusion, KTPs are predisposed to develop hyponatremia since they are exposed to immunologic, infectious, pharmacologic and oncologic disorders, the combinations of which alter their salt and water homeostatic capacity.

Impacto de la glomerulopatía post trasplante en la sobrevida del injerto renal / Post-transplant glomerulopathy impact in renal graft survival

Introducción: las glomerulopatías primarias son causa de enfermedad renal crónica en receptores de trasplante renal (30%-50%), siendo un determinante importante en la sobrevida del injerto. Recientes estudios revelan que la recurrencia fue la tercer causa más frecuente de pérdida delinjerto a 10 años de seguimiento postrasplante. Objetivo: Analizar el impacto de las glomerulopatía postrasplante como predictor de pérdida del injerto. Material y métodos: Entre enero de 1990 y abril del 2013 se realizaron 849 biopsias renales en 375 pacientes trasplantados, diagnosticándose 50 casos de glomerulopatía. Se comparó dicha población con un grupo histórico de receptores de trasplante renal entre 2000 al 2011, sin glomerulopatía. Se analizó la sobrevida del injerto renal en ambas poblaciones. Resultados: Se diagnosticaron 50 glomerulopatías post trasplante en 47 pacientes. No encontramos diferencias estadísticamente significativas entre este grupo y el grupo histórico en: edad del receptor; sexo del donante; tipo del donante; n¿²mero de miss match; tiempo de isquemia del órgano; tasa de rechazo agudo; retardo de la función del injerto; ni en la mortalidad del receptor. Si hallamos diferencias significativa en sexo masculino, 88 vs 55% (p< 0.05). La tasa de pérdida del injerto renal fue significativamente más frecuente entre los pacientes que presentaron enfermedad glomerular 38 vs 8% (p< 0.01). Conclusión: En nuestra población, la aparición de glomerulopatía post trasplante se asoció a una disminución de la sobrevida del injerto observándose una mayor tasa de pérdida en la glomerulopatía membranoproliferativa.

Introduction: primary glomerulopathy is cause of renal chronic disease in renal transplant recipients (30%-50%), being an important determinant in graft survival. Recent studies reveal that recurrence was the third most frequent cause of graft lost after 10 years post-transplant monitoring process. Objective: To analyze posttransplant glomerulopathy impact as a graft lost predictor. Methods: Between January 1990 and April 2013, 849 renal biopsies were carried out on 375 transplanted patients, 50 glomerulopathy cases were diagnosed. This population was compared with an historical renal transplant recipients group between 2000 to 2011, without glomerulopathy. Renal graft survival was analyzed in both populations. Results: 50 post-transplant glomerulopathies were diagnosed in 47 patients. We did not find statistically significant differences between this group and the historical one concerning recipient age, donor sex, donor type, miss match number, organ ischaemia time, acute rejection rate, delayed graft function, and neither in the recipient mortality. We did find significant differences in male sex, 88% vs 55% (p< 0.05). Renal graft lost rate was significantly more frequent among patients presenting glomerular disease 38 vs 8 % (p< 0.01). Conclusion: In our population, post transplant glomerulopathy was associated to graft survival reduction and a higher membranoproliferative glomerulopathy lost rate was observed.

Furosemide test in stage III-chronic kidney disease and kidney transplant patients on tacrolimus.

AIM: Furosemide test is a simple and useful test of renal physiology usually used for evaluating the capability of the collecting ducts to secrete potassium under the effect of this drug. Its behaviour pattern has already been established in healthy children, young, and old people, as well as in stage III-chronic kidney disease (III-CKD) patients. However, its behaviour has not been described in kidney transplant patients yet, which we explored in this study. MATERIALS AND METHODS: Twenty young volunteers on a standard western diet (50 mmol of potassium/day) were studied: Ten were III-CKD and the rest were kidney transplant (KT) patients on FK. Before, while the test was being carried out, and 180 min after a single dose of intravenous furosemide (1 mg/kg), urine and blood samples were obtained, for creatinine and potassium levels. From these data, we calculated fractional excretion of potassium (FEK). Statistical analysis was performed applying Wilcoxon test. RESULTS: There was a significant difference regarding pre-furosemide (basal) FE of potassium between the III-CKD and KT groups 16 ± 5 (III-CKD) versus 7 ± 5 (KT), p = 0.008. Regarding the post-furosemide, peak FEK was significantly lower in the KT group (15 ± 11 %) compared to the III-CKD ones (49.8 ± 9 %, p = 0.01). In both groups, the peak FEK post-furosemide was reached later (120 min) compared to the conventional test (30 min). CONCLUSION: Furosemide test showed significantly lower basal and post-furosemide peak FEK values in KT patients on tacrolimus compared with stage III-chronic renal disease.