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      Loin pain hematuria syndrome

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          Abstract

          Loin pain hematuria syndrome (LPHS), first described in 1967, is a rare pain syndrome, which is not well understood. The syndrome is characterized by severe intermittent or persistent flank pain, either unilateral or bilateral, associated with gross or microscopic hematuria. LPHS is a diagnosis of exclusion as there still is not a consensus of validated diagnostic criteria, though several criteria have been proposed. The wide differential diagnosis would suggest a meticulous yet specific diagnostic work-up depending on the individual clinical features and natural history. Several mechanisms regarding the pathophysiology of LPHS have been proposed but without pinpointing the actual causative etiology, the treatment remains symptomatic. Treatment modalities for LPHS are diverse including simple analgesia, opioid analgesic and kidney autotransplantation. This review article summarizes the current understanding regarding the pathophysiology of LPHS along with the steps required for proper diagnosis and a discussion of the different therapeutic approaches for LPHS.

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          Nutcracker phenomenon and nutcracker syndrome.

          Andrew K Kurklinsky, Thom W Rooke (2010)
          Nutcracker phenomenon refers to compression of the left renal vein, most commonly between the aorta and the superior mesenteric artery, with impaired blood outflow often accompanied by distention of the distal portion of the vein. The nutcracker syndrome (NCS) is the clinical equivalent of nutcracker phenomenon characterized by a complex of symptoms with substantial variations. Depending on specific manifestations, NCS may be encountered by different medical specialists. Although it may be associated with substantial morbidity, the diagnosis of NCS is often difficult and is commonly delayed. Diagnostic and treatment criteria are not well established, and the natural history of NCS is not well understood. We performed an initial review of the literature through MEDLINE, searching from 1950 to date and using the keywords nutcracker syndrome, nutcracker phenomenon, and renal vein entrapment. We performed additional reviews based on the literature citations of the identified articles. We attempted to elucidate clinical relevance of these conditions and their prominent features and to summarize professional experience.
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            Three pathways for human kidney stone formation.

            Andrew P Evan, F Coe, Elaine Worcester … (2010)
            No single theory of pathogenesis can properly account for human kidney stones, they are too various and their formation is too complex for simple understanding. Using human tissue biopsies, intraoperative imaging and such physiology data from ten different stone forming groups, we have identified at least three pathways that lead to stones. The first pathway is overgrowth on interstitial apatite plaque as seen in idiopathic calcium oxalate stone formers, as well as stone formers with primary hyperparathyroidism, ileostomy, and small bowel resection, and in brushite stone formers. In the second pathway, there are crystal deposits in renal tubules that were seen in all stone forming groups except the idiopathic calcium oxalate stone formers. The third pathway is free solution crystallization. Clear examples of this pathway are those patient groups with cystinuria or hyperoxaluria associated with bypass surgery for obesity. Although the final products may be very similar, the ways of creation are so different that in attempting to create animal and cell models of the processes one needs to be careful that the details of the human condition are included.
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              Proposed pathogenesis of idiopathic loin pain-hematuria syndrome.

              Garima Agarwal, G Molnar-Nadasdy, Dan N Spetie … (2006)
              To study loin pain-hematuria syndrome (LPHS) pathogenesis, we evaluated 43 consecutive patients for whom urological evaluation failed to disclose the cause of their recurrent flank pain and hematuria. Each underwent percutaneous kidney biopsy. In 9 patients, the biopsy specimen showed immunoglobulin A nephritis, an established cause of LPHS. We suggest these cases be designated secondary LPHS. They are not included in this analysis. The remaining patients (N = 34) are designated idiopathic (primary) LPHS. They are the basis of this report. Demographics of patients with primary LPHS are mean age of 30.8 +/- 10.3 years; 74% women; 94% white; and history of kidney stones, 47%, although none was obstructing. Primary LPHS kidney biopsy specimens showed red blood cells (RBCs) in multiple tubules, consistent with glomerular hematuria. Glomeruli were normal by means of light and immunofluorescent microscopy; however, more than 50% of biopsy specimens showed unusually thin or thick glomerular basement membranes. To assess whether the biopsy itself caused RBCs in tubules, we compared RBCs in renal tubular cross-sections from primary LPHS biopsies with those of normal kidneys (donors, n = 10). The mean percentage of tubular cross-sections containing RBCs was greater in primary LPHS than normal specimens (7.2% +/- 6.5% versus 1.6% +/- 1.0% [SD]; P < 0.0001), confirming glomerular hematuria in patients with primary LPHS. Primary LPHS pathogenesis includes glomerular hematuria, apparently from structurally abnormal glomerular basement membrane. Primary LPHS pain may be initiated by obstructing RBC casts and perhaps microcrystals in those with a history of urolithiasis. Nevertheless, other factors are needed to explain the severe pain in patients with primary LPHS.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Kidney J
                Journal ID (iso-abbrev): Clin Kidney J
                Journal ID (publisher-id): ckj
                Journal ID (hwp): ndtplus
                Title: Clinical Kidney Journal
                Publisher: Oxford University Press
                ISSN (Print): 2048-8505
                ISSN (Electronic): 2048-8513
                Publication date (Print): February 2016
                Publication date (Electronic): 07 December 2015
                Publication date PMC-release: 07 December 2015
                Volume: 9
                Issue: 1
                Pages: 128-134
                Affiliations
                [1 ]Division of Transplantation Surgery, Department of Medicine, Mayo Clinic , Rochester, MN, USA
                [2 ]Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic College of Medicine , Rochester, MN, USA
                Author notes
                Correspondence to: Mikel Prieto; E-mail: prieto.mikel@ 123456mayo.edu
                Article
                Publisher ID: sfv125
                DOI: 10.1093/ckj/sfv125
                PMC ID: 4720203
                PubMed ID: 26798473
                SO-VID: 6edee3d8-d181-436b-b414-b05721fe0b83
                Copyright © © The Author 2015. Published by Oxford University Press on behalf of ERA-EDTA.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 10 August 2015
                Date accepted : 29 October 2015
                Categories
                Subject: Contents
                Subject: Chronic Kidney Disease

                ScienceOpen disciplines: Nephrology
                Keywords: autotransplant,flank pain,hematuria,loin pain hematuria syndrome
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: autotransplant, flank pain, hematuria, loin pain hematuria syndrome

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