Scintigraphy and Doppler ultrasonography for the evaluation of obstructive urinary calculi

Forty-seven patients with unilateral obstructive calculi (12 males and 35 females) were submitted to 99mTc-diethylene triamine pentaacetic acid (DTPA) or 99mTc-dimercaptosuccinic acid (DMSA) scans for assessment of renal function. The scans revealed unilateral functional deficit in 68 and 66% of the patients, respectively. A calculus size of 1.1 to 2.0 cm was significantly associated with deficit detected by DTPA, but duration of obstruction and calculus localization were not. After relief of the obstruction, the mean percent renal function of the affected kidney was found to be significantly increased from 25 ± 12% to 29 ± 12% in DTPA and from 21 ± 15% to 24 ± 12% in DMSA. Initial Doppler ultrasonography performed in 35 patients detected an increased resistive index in 10 (29%). In the remaining patients with a normal resistive index, ureteral urinary jet was observed, indicating partial obstruction. The high frequency of renal function impairment detected by DTPA and of tubulointerstitial damage detected by DMSA as well as the slight amelioration of unilateral renal function after relief of obstruction suggest that scintigraphy assessment may help evaluate the unilateral percentage of renal function and monitor renal function recovery when it occurs. The presence of a urinary jet detected by Doppler ultrasonography further indicates the severity of obstruction and the recovery prognosis.Universidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Divisão de NefrologiaUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Divisão de Medicina NuclearUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Divisão de UltrassonografiaUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Divisão de UrologiaUNIFESP, EPM, Divisão de NefrologiaUNIFESP, EPM, Divisão de Medicina NuclearUNIFESP, EPM, Divisão de UltrassonografiaUNIFESP, EPM, Divisão de UrologiaSciEL

Pre-Transplant Hyperparathyroidism and Graft or Patient Outcomes After Kidney Transplantation

The impact of pre-transplant parathyroid hormone (PTH) levels on early or long-term kidney function after kidney transplantation is subject of debate. We assessed whether severe hyperparathyroidism is associated with delayed graft function (DGF), death-censored graft failure (DCGF), or all-cause mortality. In this single-center cohort study, we studied the relationship between PTH and other parameters related to bone and mineral metabolism, including serum alkaline phosphatase (ALP) at time of transplantation with the subsequent risk of DGF, DCGF and all-cause mortality using multivariable logistic and Cox regression analyses. In 1,576 kidney transplant recipients (51.6 ± 14.0 years, 57.3% male), severe hyperparathyroidism characterized by pre-transplant PTH ≥771 pg/mL (>9 times the upper limit) was present in 121 patients. During 5.2 [0.2–30.0] years follow-up, 278 (15.7%) patients developed DGF, 150 (9.9%) DCGF and 432 (28.6%) died. A higher pre-transplant PTH was not associated with DGF (HR 1.06 [0.90–1.25]), DCGF (HR 0.98 [0.87–1.13]), or all-cause mortality (HR 1.02 [0.93–1.11]). Results were consistent in sensitivity analyses. The same applied to other parameters related to bone and mineral metabolism, including ALP. Severe pre-transplant hyperparathyroidism was not associated with an increased risk of DGF, DCGF or all-cause mortality, not supporting the need of correction before kidney transplantation to improve graft or patient survival

Metabolic diagnosis and medical prevention of calcium nephrolithiasis and its systemic manifestations: a consensus statement

Background: Recently published guidelines on the medical management of renal stone disease did not address relevant topics in the field of idiopathic calcium nephrolithiasis, which are important also for clinical research. Design: A steering committee identified 27 questions, which were proposed to a faculty of 44 experts in nephrolithiasis and allied fields. A systematic review of the literature was conducted and 5216 potentially relevant articles were selected; from these, 407 articles were deemed to provide useful scientific information. The Faculty, divided into working groups, analysed the relevant literature. Preliminary statements developed by each group were exhaustively discussed in plenary sessions and approved. Results: Statements were developed to inform clinicians on the identification of secondary forms of calcium nephrolithiasis and systemic complications; on the definition of idiopathic calcium nephrolithiasis; on the use of urinary tests of crystallization and of surgical observations during stone treatment in the management of these patients; on the identification of patients warranting preventive measures; on the role of fluid and nutritional measures and of drugs to prevent recurrent episodes of stones; and finally, on the cooperation between the urologist and nephrologist in the renal stone patients. Conclusions: This document has addressed idiopathic calcium nephrolithiasis from the perspective of a disease that can associate with systemic disorders, emphasizing the interplay needed between urologists and nephrologists. It is complementary to the American Urological Association and European Association of Urology guidelines. Future areas for research are identified

BONE-DISEASE IN CALCIUM STONE FORMING PATIENTS

The association between idiopathic hypercalciuria and osteopenia (OF) has been recently recognized. It is not established whether or not calcium intake plays a critical role in the loss of bone mass. Fifty-five calcium stone forming patients with either absorptive hypercalciuria (AH) or fasting hypercalciuria (FH), 29 males and 26 premenopausal females, were submitted to dual photon absorptiometry at lumbar spine. Calcium intake was assessed by a 72 hr dietary record. OP was detected in 20% (11/55) of patients, being more common among men, 9/26 (35%) than in women, 2/29 (7%), p < 0.05. Male FH patients presented lower mean bone mineral density (BMD) than sex, weight and age-matched control(1.058 +/- 0.18 vs 1.209 +/- 0.13 g/cm(2), X +/- SD, p < 0.05). OP was more frequent in FH patients, 7/20 (35%) than in AH patients 4/35 (11%), albeit the difference was not statistically significant. There was no correlation between calcium intake and BMD measurement. Six osteopenic male FH patients were further submitted to histomorphometric evaluation with tetracycline double labeling. Bone volume was lower than the controls (13.2 +/- 3.0 vs 27.2 +/- 3.7%, p < 0.05). Osteoid surfaces were reduced, although not significantly (10.1 +/- 8.2% vs 15.9 +/- 6.7%). Eroded surfaces were markedly increased (23.9 +/- 13.4 vs 4.2 +/- 1.4%, p < 0.05). The bone formation rate was very low with a complete lack of tetracycline double labeling in 4 patients. These data suggest low bone volume, tendency to low bone formation, increased bone resorption and a severe mineralization defect, consistent with normal or low bone turnover osteoporosis.ESCOLA PAULISTA MED,DIV NEPHROL,BR-04023062 SAO PAULO,BRAZILESCOLA PAULISTA MED,DIV NEPHROL,BR-04023062 SAO PAULO,BRAZILWeb of Scienc

Phosphate and FGF-23 homeostasis after kidney transplantation

Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs. By 3-12 months after transplantation, phosphate homeostasis is at least partially restored in the majority of recipients, which is paralleled by a substantially reduced risk of cardiovascular-associated morbidity and mortality compared with the pre-transplantation setting. Many renal transplant recipients, however, exhibit persistent abnormalities in phosphate homeostasis, which is often due to multifactorial causes, and may contribute to adverse outcomes on the cardiovascular system, kidney, and bone. Dietary and pharmacologic interventions might improve phosphate homeostasis in renal transplant recipients, but additional insight into the pathophysiology of transplantation-associated abnormalities in phosphate homeostasis is needed to further optimize disease management and improve prognosis for renal transplant recipients