Renal Transplantation in Patients Older Than 60 Years With High Comorbidity. Is There a Survival Benefit? A Multicenter Study in Argentina.

BACKGROUND: The impact of renal transplantation (RT) in the elderly with many comorbid conditions is a matter of concern. The aim of our study was to assess the impact of RT on the survival of patients older than 60 years compared with those remaining on the waiting list (WL) according to their comorbidities. METHODS: In this multicentric observational retrospective cohort study, we included all patients older than 60 years old admitted on the WL from 01 January 2006 to 31 December 2016. The Charlson comorbidity index (CCI) score was calculated for each patient at inclusion on the WL. Kidney donor risk index was used to assess donor characteristics. RESULTS: One thousand and thirty-six patients were included on the WL of which 371 (36%) received an RT during a median follow-up period of 2.5 (1.4-4.1) years. Patient survival was higher after RT compared to patients remaining on the WL, 87%, 80%, and 72% versus 87%, 55%, and 30% at 1, 3, and 5 years, respectively. After RT survival at 5 years was 37% higher for patients with CCI ≥ 3, and 46% higher in those with CCI < 3, compared with patients remaining on the WL. On univariate and multivariate analysis, patient survival was independently associated with a CCI of ≥3 (hazard ratio 1.62; confidence interval 1.09-2.41; P < 0.02) and the use of calcineurin-based therapy maintenance therapy (hazard ratio 0.53; confidence interval 0.34-0.82; P < 0.004). CONCLUSIONS: Our study showed that RT improved survival in patients older than 60 years even those with high comorbidities. The survival after transplantation was also affected by comorbidities.

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.

Aging Kidney Transplantation.

There are several immunological and non-immunological factors related to renal graft deterioration, and histological lesions such as interstitial fibrosis and tubular atrophy overlap with those observed in aging kidneys. Consequently, it has been proposed that kidney transplant senescence could contribute to graft loss. The process of cell senescence displays characteristics such as an increased expression of specific aging suppressor genes, shortened telomeres, mitochondrial changes, increased expression of negative regulators of the cell cycle, and immunological senescence. Additionally, tubular frailty characterizes the aged kidney, making it more susceptible to ischemia, reperfusion, toxic injury, and consequently, to inflammation. Moreover, renal tissue injury predisposes the older graft not only to progressive deterioration due to glomerular hyperfiltration, but also triggers acute rejection due to increased immunogenicity. In conclusion, renal graft senescence is a complex process, and its better understanding will help the nephrologist in its management in order to achieve a longer graft survival.

Hiperuricemia, enfermedad renal crónica y trasplante renal (parte II) / Hyperuricemia, chronic renal disease and renal transplant (part II)

La hiperuricemia (HU) en el trasplante renal (TR) ha sido definida igual que en la población general en las Guías KDIGO como valores por encima de 6 mg/dl en mujeres y 7 mg/dl en hombres. La incidencia de HU en algunas poblaciones es de 28%,(1) alcanzando el 80% en la era Ciclosporina (CSA).(2) La HU se observa precozmente luego del TR, los factores de riesgo asociados con su desarrollo incluyen: edad avanzada al momento del TR; historia de gota o HU pre-existente; obesidad; presencia de síndrome metabólico (SM); deterioro de la función del injerto; uso de inmunosupresores, principalmente ciclosporina (CSA); uso de diuréticos

Hyperuricemia (HU) in renal transplant (RT) has been defined, like general population, with KDIGO Guides, as over 6 mg/dl values in women and 7 mg/dl in men. HU incidence in some populations are 28%, reaching 80% in Cyclosporine era (CSA). HU is early observed after RT, risk factors associated with its development include: advanced age at the time of RT; gout history or pre-existing HU; obesity; metabolic syndrome presence (MS); graft function deterioration; use of Inmunosuppression drugs, mainly cyclosporine (CSA); use of diuretics

Hiperuricemia, enfermedad renal crónica y trasplante renal (parte ii) / Hyperuricemia, chronic kidney disease and kidney transplant (part ii)

La hiperuricemia post trasplante ha sido definida con valores iguales a la población general, en su prevalencia pueden alcanzar un 80% en los que ha recibido un trasplante renal, un 5-25% desarrolla crisis gotosas. La edad avanzada al momento del implante, la historia de hiperuricemia o gota, la obesidad, el tratamiento con anticalcineurínicos, el uso de diuréticos y el bajo filtrado glomerular son algunos de los factores implicados en su desarrollo. La hiperuricemia se han relacionado con disminución de la vasodilatación mediada por óxido nítrico y la proliferación del músculo liso vascular a través de efectos proinflamatorios y profibróticos (mediados por células T, macrófagos, PDGF, TGF ² , entre otros). Estos efectos se han asociado a su vez con hipertensión arterial, afecciones cardiovasculares y progresión del daño renal (relacionado con fibrosis túbulo intersticial, arterioloesclerosis de la aferente, atrofia tubular), factores que conllevan a una reducción en la sobrevida del injerto como del paciente. La indicación de tratamiento de la hiperuricemia asintomática en esta población es aún objeto de debate, tanto respecto de la indicación en sí como del tipo de fármaco a utilizar, a diferencia de lo que ocurre en litiasis, tofos o artritis donde se debe encarar el tratamiento, jerarquizando la interacción con las drogas propias del trasplante. Se debe considerar que la mayoría de la información disponible se desprende del análisis sobre población general por lo que se requieren estudios de este grupo poblacional en particular.

Post-transplant hyperuricemia has been defined with equal values to the ones of general population, its prevalence can reach 80% in those who have received a kidney transplant, and 5 to 25% can develop gout crisis. Advanced age at implant, history of hyperuricemia or gout, obesity, treatment with calcineurin inhibitors, use of diuretics and low glomerular filtration rate are some of the factors involved in its development. Hyperuricemia has been linked to decreased nitric oxide mediated vasodilation and proliferation of vascular smooth muscle through proinflammatory and profibrotic effects (mediated by T cells, macrophages, PDGF, TGF ² among others). These effects have been associated, in turn, with hypertension, cardiovascular disease and renal damage progression (related tubulointerstitial fibrosis, arteriosclerosis of afferent tubular atrophy) factors that lead to a reduction in graft and patient survival. Indication for asymptomatic hyperuricemia treatment in this population is still under debate, both in terms of the indication in itself and the type of drug used, unlike what happens in stones, arthritis, or tophi where they must face treatment must be addressed, prioritizing the interaction with the drugs used in transplantation. It must be considered that most of the available information comes from the analysis of general population, therefore studies on this population group are particularly required.

Hiperuricemia, enfermedad renal crónica y trasplante renal (parte I) / Hyperuricemia, chronic kidney disease and kidney transplant (part I)

La hiperuricemia post trasplante ha sido definida con valores iguales a la población general, en su prevalencia pueden alcanzar un 80% en los que han recibido un trasplante renal, un 5-25% desarrolla crisis gotosas. La edad avanzada al momento del implante, la historia de hiperuricemia o gota, la obesidad, el tratamiento con anticalcineurínicos, el uso de diuréticos y el bajo filtrado glomerular son algunos de los factores implicados en su desarrollo. La hiperuricemia se han relacionado con disminución de la vasodilatación mediada por óxido nítrico y la proliferación del músculo liso vascular a través de efectos proinflamatorios y profibróticos (mediados por células T, macrófagos, PDGF, TGF ß, entre otros). Estos efectos se han asociado a su vez con hipertensión arterial, afecciones cardiovasculares y progresión del daño renal (relacionado con fibrosis túbulo intersticial, arterioloesclerosis de la aferente, atrofia tubular), factores que conllevan a una reducción en la sobrevida del injerto como del paciente. La indicación de tratamiento de la hiperuricemia asintomática en esta población es aún objeto de debate, tanto respecto de la indicación en sí como del tipo de fármaco a utilizar, a diferencia de lo que ocurre en litiasis, tofos o artritis donde se debe encarar el tratamiento, jerarquizando la interacción con las drogas propias del trasplante. Se debe considerar que la mayoría de la información disponible se desprende del análisis sobre población general por lo que se requieren estudios de este grupo poblacional en particular.

Post-transplant hyperuricemia has been defined with equal values to the ones of general population, its prevalence can reach 80% in those who have received a kidney transplant, and 5 to 25% can develop gout crisis. Advanced age at implant, history of hyperuricemia or gout, obesity, treatment with calcineurin inhibitors, use of diuretics and low glomerular filtration rate are some of the factors involved in its development. Hyperuricemia has been linked to decreased nitric oxide mediated vasodilation and proliferation of vascular smooth muscle through proinflammatory and profibrotic effects (mediated by T cells, macrophages, PDGF, TGF ß among others). These effects have been associated, in turn, with hypertension, cardiovascular disease and renal damage progression (related tubulointerstitial fibrosis, arteriosclerosis of afferent tubular atrophy) factors that lead to a reduction in graft and patient survival. Indication for asymptomatic hyperuricemia treatment in this population is still under debate, both in terms of the indication in itself and the type of drug used, unlike what happens in stones, arthritis, or tophi where they must face treatment must be addressed, prioritizing the interaction with the drugs used in transplantation. It must be considered that most of the available information comes from the analysis of general population, therefore studies on this population group are particularly required

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.

Fractional excretion of K, Na and Cl following furosemide infusion in healthy, young and very old people.

UNLABELLED: Furosemide test is a simple and useful test of renal physiology used to evaluate the capability of the collecting ducts to secrete potassium under the effect of serum aldosterone. Its behaviour pattern has been established in children and young adults but not described in very old healthy people, which we explored in this study. MATERIAL AND METHODS: Twenty-six healthy volunteers on a standard Western diet (50 mmol of K/day) were studied: 20 of them were young (between 17 and 40 years old) and the rest were very old (between 75 and 85 years old). They suffered from no diseases and were not on any medication. Before, during the test and 180 min after a single dose of intravenous furosemide (1 mg/kg), urine and blood samples were obtained for creatinine and electrolytes levels. From these data we calculated fractional excretion (FE) of electrolytes; serum aldosterone was measured pre and post furosemide infusion. Statistical analysis was performed by applying Student's t-test. RESULTS: There was no significant difference regarding pre-furosemide (basal) FE of potassium between the very old and young group. Post-furosemide average FE of potassium was significantly lower in the very old group (27.4 +/- 2%) compared with the young group (35.4 +/- 9%) (P = 0.04). Even though there was no significant difference in post-furosemide peak FE of potassium value, it was reached later in the very old (120 min) compared with the young (30 min). Serum aldosterone levels were significantly higher post furosemide in both groups: 18.3 +/- 12.2 ng/dl (pre) versus 32.5 +/- 18.6 ng/dl (post) in the young (P = 0.007) and 69.8 +/- 13.7 ng/dl (pre) versus 113.3 +/- 54.8 ng/dl (post) in the very old (P = 0.04). Furthermore, all serum aldosterone values (pre and post furosemide) were significantly higher in very old people compared with young people (P < 0.001). Basal fractional excretion of sodium and chloride were slightly higher in the very old group compared with the young group (P = 0.05). Average post-furosemide FE of sodium and chloride were slightly and significantly lower in the very old (P = 0.05 and P = 0.03), respectively. However, there was no significant difference in peak post-furosemide FE of sodium and chloride values, which were reached later in the very old (120 min) compared with the young (30 min). CONCLUSION: Furosemide test showed a significantly lower average post-furosemide FE of potassium value, delayed post-furosemide peak FE of Na, K and Cl and a hormonal pattern of aldosterone resistance in very old people.

Renal physiology in elderly persons with severe immobility syndrome.

OBJECTIVE: The immobility syndrome (IS) is a common condition in the elderly and consists of a reduction in the capacity to perform daily activities because of motor function deterioration. This syndrome leads to characteristic structural and physiological changes in the body, but renal physiology studies have not been conducted on this population. For this reason, we decided to study prospectively changes in renal function in these individuals. MATERIAL AND METHODS: We enrolled into this study 17 volunteers over 64 years of age, all of whom lived in the same nursing home. The patients were divided into two groups: nine healthy mobile persons and eight others who suffered from severe IS. Exclusion criteria were the presence of any disease or use of any drug that could induce water and electrolytes alteration. Blood and urine samples were drawn to measure sodium, potassium, creatinine, urea, calcium, phosphorus, magnesium, and uric acid in order to obtain their fractional excretion. Plasma osmolality and vasopressin were also measured. Total body water and lean body mass were obtained by bioelectrical impedance analysis. Statistical analysis was performed applying Student's t-test (P = 0.01) and Pearson's correlation test. RESULTS: A significant difference in body water composition was found between the groups. Thus in the IS group plasma sodium level was slightly lower and total water content was significantly higher than in the mobile subjects: 140 +/- 5 vs. 143 +/- 1 mmol/l (P = 0.01); 61 +/- 8% vs. 50 +/- 10% (P < 0.001), respectively. Despite these differences, plasma osmolality and vasopressin values were within the normal range in both groups. However, there was a good positive correlation between these two variables in the mobile group only: R 0.9 (mobile) vs. R -0.2 (immobile). We found no significant difference in plasma creatinine or fractional excretion of sodium, potassium, calcium, phosphorus, magnesium, urea, and uric acid between the groups. CONCLUSION: Total body water content was significantly higher in the elderly who suffered from severe immobility syndrome than in healthy mobile elderly. In contrast with the mobile group, for which there was a good positive correlation between plasma osmolality and plasma vasopressin, for individuals with IS there was no correlation between plasma osmolality and plasma vasopressin.

Litiasis renal

Esta obra ayuda de manera escueta, la patología renal y sus complicaciones, como por ejemplo: Cálculos renales, coólicos, diagnostico y tratamiento

Prevalencia de hipercalcemia en pacientes con transplante [sic] renal: factores predictores / Prevalence of hypercalcemia in patients with renal transplant: predictive factors

El transplante renal (TxR) mejora el hiperparatiroidismo urémico. Sin embargo algunos pacientes pueden presentar hipercalcemia en el post TxR que altera la función del injerto y requiere en muchos casos cirugía de la paratiroides. El objetivo del trabajo fue establecer la prevalencia de hipercalcemia en pacientes con TxR y los factores que la predicen. Se incluyeron 60 adultos con insuficiencia renal crónica que recibieron un transplante renal. Se consignaron los valores de Calcemia, Fosfatemia, Fosfatasa alcalina y PTH intacta, previo al transplante y durante el seguimiento posterior. Se subdividió a la población en tres grupos según la calcemia post transplante y su duración en el período de un año: pacientes con 1. Calcemia normal (NC); 2. Hipercalcemia transitoria (HT) (se normaliza antes del año del transplante); 3. Hipercalcemia persistente (HP) (hipercalcemia sostenida más de 12 meses y que se adscribe a disfunción paratiroidea). Se verificó hipercalcemia post-transplante en el 33,4% de los pacientes (16,7% con HP y 16,7% con HT). Los factores asociados a hipercalcemia persistente fueron: 1) Mayor tiempo de hemodiálisis (NC: 30,5±4,8 meses; HT: 45,4±11,7 meses y HP: 64,7±14,0 meses; ANOVA: p=0,02); 2) Calcemias elevadas (NC: 9,4±0,1 mg/dl, HT: 10,2±0,3mg/dl y HP: 10,3±0,4 mg/dl; ANOVA: p=0,002) y PTH pre TxR (NC: 202 (78-485) pg/ml; HT: 146 (115-508) pg/ml y HP: 759 (368-1126) pg/ml; mediana 1er-3er cuartilo, test de Kruskall-Wallis: p=0,02). Se comprobaron correlaciones positivas entre tiempo de hemodiálisis y PTH post TxR (r=0,65; p<0,05) y Ca post TxR (r=0,32; p=0,02); la PTH pre y post TxR correlacionaron en forma directa (r=0,55; p<0,05). El grupo de pacientes con hipercalcemia transitoria presentó calcemias superiores a las óptimas con niveles de PTH adecuados. Los niveles de calcio y PTH elevados en pacientes en diálisis se asocian al desarrollo de hipercalcemia persistente en el período posterior al TxR.

Correlation between creatinine clearance and transtubular potassium concentration gradient in old people and chronic renal disease patients.

Senescence and chronic kidney disease (CKD) reduce progressively glomerular filtration rate (GFR), which usually results in an increase in potassium renal secretion. To evaluate whether the transtubular potassium concentration gradient (TTKG) is more accurate parameter for evaluating the renal secretion of this cation than using fractional excretion of potassium as its urinary secretion marker, we studied 55 subjects, 43 of them were healthy elderly volunteers and 12 were CKD patients. Exclusion criteria were: abnormal plasma potassium level or presence of any disease or drug that could induce alteration of balance of this electrolyte levels. All the subjects were on a diet with a potassium content around 50 mmol/day. The curves, which demonstrate the relationship between creatinine clearance and TTKG and the grade of correlation between these two parameters were analyzed in both groups. We found that the transtubular potassium concentration gradient had a significant negative correlation with the creatinine clearance level in the healthy elderly group, while there was no correlation in the CKD group.

Hyperkalemia associated to hepatitis in a peritoneal dialysis patient.

Hyperkalemia is an unusual complication in peritoneal dialysis patients, having a prevalence of around 0.8% among the continuous ambulatory peritoneal dialysis (CAPD) population. The main cause of hyperkalemia in this group is the release of potassium from sources such as gross haematomas and rhabdomyolysis. However, there is no previous report regarding hyperkalemia induced by intracellular potassium shift into the intravascular compartment secondary to drug-induced acute hepatitis in peritoneal dialysis. We present the following case report of a peritoneal dialysis patient, well dialyzed and on a low-potassium diet, who was admitted in our hospital with paralysis secondary to hyperkalemia (serum potassium: 7 mmol/l). Both disorders disappeared using continuous automated peritoneal dialysis (APD) until liver enzymes normalized. We concluded that acute hepatitis can be a cause of hyperkalemia in a properly nourished and well-dialyzed peritoneal dialysis patient.

Transtubular potassium concentration gradient: comparison between healthy old people and chronic renal failure patients.

UNLABELLED: Transtubular potassium concentration gradient (TTKG) is an index of potassium secretory activity in the distal tubule. Since water reabsorption takes place in the distal tubule as well, urine potassium concentration is a less accurate index evaluating distal K+ secretion because the effect of water is not taken into account on urine potassium concentrations. Potassium secretion and water reabsorption are strongly related to age and renal function. As a consequence, TTKG would be altered in both elderly individuals, as well as in patients with chronic renal failure (CRF). The aim of this study was to assess and compare TTKG in these two groups. PATIENTS & METHODS: A total of 55 individuals were studied, 12 of them were patients with CRF and 43 healthy elderly subjects with normal renal function. Informed consent was obtained from all patients. Patients with diabetes mellitus, cardiac failure, cirrhosis, obstructive uropathy, hyperkalemia, hypokalemia, or taking any medication that could alter the potassium balance were excluded from the study. All subjects were on a diet containing 50 mmol of potassium intake daily (documented by a three-day dietary record). Plasma potassium, creatinine, urea, glucose and osmolality were measured in all as well. 24 h creatinine clearance (CrCl ) and TTKG were calculated. Statistical analysis was made using Student's t-test. RESULTS: TTKG was significantly lower in the elderly group (4.2+/-1.9 vs 6.2+/-1.8 , P 0.005)Both groups had a significantly lower TTKG when compared to healthy young people (8+/-2). Plasma and urine potassium levels, as well as plasma osmolality were similar in the two groups. Only urine osmolality was lower in the CRF group (382+/-141 vs. 514+/-180, P=0.01) CONCLUSION: Both old age and renal impairment lead to a reduced TTKG in comparison with young healthy people. Furthermore, TTKG is significantly lower in elderly healthy subjects compared to patients with CRF.

Cutaneous necrosis by calcific uremic arteriolopathy.

BACKGROUND: Calcific uremic arteriolopathy is a rare and serious disorder characterized by systemic medial calcification of the arteries and tissue ischemia. Most often it is found in patients with chronic renal failure on dialysis and in renal transplant recipients with secondary hyperparathyroidism. METHODS: We report six patients with end-stage renal disease [five on hemodialysis (one with a nonfunctioning renal graft) and one on peritoneal dialysis] who developed painful livedo reticularis and skin necrosis of the limbs. All had secondary hyperparathyroidism and elevated calcium-phosphorus product. Our patients presented with the following clinical features: white race (six patients), hypoalbuminemia (three patients), diabetes (one patient), and obesity (four patients). RESULTS: Subtotal parathyroidectomy was performed in three cases. Despite this procedure, two patients died; one patient survived and his lesions healed. One patient was treated with aggressive wound care and hemodialysis (with low dialysate calcium concentration and Renagel phosphorus binders) and one patient received only local wound care, both with improvement of their lesions. In one case, no therapy was performed because the patient died immediately after diagnosis. CONCLUSIONS: The three patients who survived (Cases 4, 5 and 6) had distal lesions, normal serum albumin, and an early diagnosis. There was a relationship between the outcome of the patients and these factors, rather than the type of treatment received.

Alteraciones en la actividad del calcio-magnesio ATPasa en la membrana de los eritrocitos en pacientes litiasicos con hipercalciuria / Alterations in the calcium-magnesium activity ATPase in the membrane of the erytrosites in lithiasic patients with hypercalciuria

La CaMgATPasa es una enzima involucrada en los movimientos de calcio a través de las membranas biológicas. Nosotros testeamos la actividad de dicha enzima en membranas de eritrocitos de 17 pacientes hipercalciúricos y la comparamos con 8 controles sanos. Los pacientes con hipercalciuria tuvieron una actividad de CaMgATPasa que fue significativamente superior a los controles (18,02 2,83 vs 14,69 1,78 nM . mg-1 p<0,01). La excreción de urinaria de calcio en 24 hs (UCa.V) estuvo directa y significativamente relacionada con la actividad de la enzima (UCa.V: 36,31 x CaMgATPasa - 371,08 r:0,65 p<0,05) sólo en pacientes con hipercalciuria. Cuando agrupamos los pacientes acorde al diagnóstico fisiopatológico en hipercalciuria absortiva (HCA) e hipercalciuria renal (HCRT) encontramos que la actividad enzimática estuvo sólo significativamente elevada en aquellos portadores de HCA al compararlos con los controles (19,17 3,49 vs 14,68 1,79 nM . mg-1 .min-1 p<0,025).No encontramos diferencias estadísticamente significativas entre HCRT y controles (16,83 1,99nM . mg-1 . min-1; p:NS) y en HCRT vs HCA (p<0,14). Concluimos que las alteraciones en el transporte de calcio en la hipercalciuria dependería de anormalidades en la actividad de la CaMgATPasa