Browsing by Author "Goldfarb, David S."

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    Metabolic diagnosis and medical prevention of calcium nephrolithiasis and its systemic manifestations: a consensus statement
    (Springer-Verlag, 2016-12) Gambaro, Giovanni; Croppi, Emanuele; Coe, Fredric; Lingeman, James; Moe, Orson; Worcester, Elen; Buchholz, Noor; Bushinsky, David; Curhan, Gary C.; Ferraro, Pietro Manuel; Fuster, Daniel; Goldfarb, David S.; Heilberg, Ita Pfeferman; Hess, Bernard; Lieske, John; Marangella, Martino; Milliner, Dawn; Preminger, Glen M.; Reis Santos, Jose’ Manuel; Sakhaee, Khashayar; Sarica, Kemal; Siener, Roswitha; Strazzullo, Pasquale; Williams, James C.; Department of Urology, School of Medicine
    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.
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    Tamm-Horsfall protein/uromodulin deficiency elicits tubular compensatory responses leading to hypertension and hyperuricemia
    (American Physiological Society, 2018-06-01) Liu, Yan; Goldfarb, David S.; El-Achkar, Tarek M.; Lieske, John C.; Wu, Xue-Ru; Medicine, School of Medicine
    Expression of Tamm-Horsfall protein (THP or uromodulin) is highly restricted to the kidney thick ascending limb (TAL) of loop of Henle. Despite the unique location and recent association of THP gene mutations with hereditary uromodulin-associated kidney disease and THP single nucleotide polymorphisms with chronic kidney disease and hypertension, the physiological function(s) of THP and its pathological involvement remain incompletely understood. By studying age-dependent changes of THP knockout (KO) mice, we show here that young KO mice had significant salt and water wasting but were partially responsive to furosemide, due to decreased luminal translocation of Na-K-Cl cotransporter 2 (NKCC2) in the TAL. Aged THP KO mice were, however, markedly oliguric and unresponsive to furosemide, and their NKCC2 was localized primarily in the cytoplasm as evidenced by lipid raft floatation assay, cell fractionation, and confocal and immunoelectron microscopy. These aged KO mice responded to metolazone and acetazolamide, known to target distal and proximal tubules, respectively. They also had marked upregulation of renin in juxtaglomerular apparatus and serum, and they were hypertensive. Finally, the aged THP KO mice had significant upregulation of Na-coupled urate transporters Slc5a8 and Slc22a12 as well as sodium-hydrogen exchanger 3 (NHE3) in the proximal tubule and elevated serum uric acid and allantoin. Collectively, our results suggest that THP deficiency can cause progressive disturbances in renal functions via initially NKCC2 dysfunction and later compensatory responses, resulting in prolonged activation of the renin-angiotensin-aldosterone axis and hyperuricemia.
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    Urine and stone analysis for the investigation of the renal stone former: a consensus conference
    (SpringerLink, 2021-02) Williams, James C., Jr.; Gambaro, Giovanni; Rodgers, Allen; Asplin, John; Bonny, Olivier; Costa-Bauzá, Antonia; Ferraro, Pietro Manuel; Fogazzi, Giovanni; Fuster, Daniel G.; Goldfarb, David S.; Grases, Félix; Heilberg, Ita P.; Kok, Dik; Letavernier, Emmanuel; Lippi, Giuseppe; Marangella, Martino; Nouvenne, Antonio; Petrarulo, Michele; Siener, Roswitha; Tiselius, Hans-Göran; Traxer, Olivier; Trinchieri, Alberto; Croppi, Emanuele; Robertson, William G.; Anatomy and Cell Biology, School of Medicine
    The Consensus Group deliberated on a number of questions concerning urine and stone analysis over a period of months, and then met to develop consensus. The Group concluded that analyses of urine and stones should be routine in the diagnosis and treatment of urinary stone diseases. At present, the 24-h urine is the most useful type of urine collection, and accepted methods for analysis are described. Patient education is also important for obtaining a proper urine sample. Graphical methods for reporting urine analysis results can be helpful both for the physician and for educating the patient as to proper dietary changes that could be beneficial. Proper analysis of stones is also essential for diagnosis and management of patients. The Consensus Group also agreed that research has shown that evaluation of urinary crystals could be very valuable, but the Group also recognizes that existing methods for assessment of crystalluria do not allow this to be part of stone treatment in many places.