Proposed Pathogenesis of Idiopathic Loin Pain–Hematuria Syndrome

Spetie, Dan N.; Nádasdy, Tibor; Nadasdy, Gyongyi; Agarwal, Garima; Mauer, Michael; Agarwal, Anil; Khabiri, Hooman; Nagaraja, Haikady N.; Nahman, N. S.; Hartman, John M.; Hebert, Lee A.

doi:10.1053/j.ajkd.2005.11.029

Cited by 55 publications

(57 citation statements)

References 27 publications

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“…There was no evidence of crescents, mesangial proliferation, or interstitial hemorrhage. A high prevalence of hypercalciuria, hyperuricosuria, and nephrolithiasis has been found among patients with TBMD and loin-pain hematuria syndrome (23,24). Gross hematuria and loin-pain episodes could be related to these abnormalities.…”

Section: Macroscopic Glomerular Hematuria and Akimentioning

confidence: 98%

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AKI Associated with Macroscopic Glomerular Hematuria

Moreno

Martín-Cleary

Gutiérrez

et al. 2012

Clinical Journal of the American Society of Nephrology

119

110

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SummaryHematuria is a common finding in various glomerular diseases. This article reviews the clinical data on glomerular hematuria and kidney injury, as well as the pathophysiology of hematuria-associated renal damage. Although glomerular hematuria has been considered a clinical manifestation of glomerular diseases without real consequences on renal function and long-term prognosis, many studies performed have shown a relationship between macroscopic glomerular hematuria and AKI and have suggested that macroscopic hematuria-associated AKI is related to adverse long-term outcomes. Thus, up to 25% of patients with macroscopic hematuriaassociated AKI do not recover baseline renal function. Oral anticoagulation has been associated with glomerular macrohematuria-related kidney injury. Several pathophysiologic mechanisms may account for the tubular injury found on renal biopsy specimens. Mechanical obstruction by red blood cell casts was thought to play a role. More recent evidence points to cytotoxic effects of oxidative stress induced by hemoglobin, heme, or iron released from red blood cells. These mechanisms of injury may be shared with hemoglobinuria or myoglobinuria-induced AKI. Heme oxygenase catalyzes the conversion of heme to biliverdin and is protective in animal models of heme toxicity. CD163, the recently identified scavenger receptor for extracellular hemoglobin, promotes the activation of anti-inflammatory pathways, opening the gates for novel therapeutic approaches.

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Section: Macroscopic Glomerular Hematuria and Akimentioning

confidence: 98%

“…Gross hematuria and loin-pain episodes could be related to these abnormalities. Although not specifically investigated, it is generally thought that hypercalciuria and hyperuricosuria could induce the formation of intraluminal microcrystals causing tubular damage and nonglomerular bleeding (23,24).…”

Section: Macroscopic Glomerular Hematuria and Akimentioning

confidence: 99%

AKI Associated with Macroscopic Glomerular Hematuria

Moreno

Martín-Cleary

Gutiérrez

et al. 2012

Clinical Journal of the American Society of Nephrology

119

110

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“…More frequent in females (70%), LPHS presents with recurrent haematuria by the third decade of life. The electron microscopy showed abnormally thin or thick GBM [49] . It has been proposed that abnormalities on GBM allow RBCs leak into the urinary space causing intratubular obstruction and clots.…”

Section: Primary Gbm Disordersmentioning

confidence: 99%

Pathogenesis of glomerular haematuria

Yuste

Gutiérrez

Sevillano

et al. 2015

WJN

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Haematuria was known as a benign hallmark of some glomerular diseases, but over the last decade, new evidences pointed its negative implications on kidney disease progression. Cytotoxic effects of oxidative stress induced by hemoglobin, heme, or iron released from red blood cells may account for the tubular injury observed in human biopsy specimens. However, the precise mechanisms responsible for haematuria remain unclear. The presence of red blood cells (RBCs) with irregular contours and shape in the urine indicates RBCs egression from the glomerular capillary into the urinary space. Therefore glomerular haematuria may be a marker of glomerular filtration barrier dysfunction or damage. In this review we describe some key issues regarding epidemiology and pathogenesis of haematuric diseases as well as their renal morphological findings.

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“…Of the 10 reported patients, only 4 experienced recovery of kidney function. Those at risk for this form of AKI appear to be those who are predisposed to glomerular hemorrhage, either because the have abnormalities of glomerular membrane basement membrane width [2,3,4,5] or chronic kidney disease (CKD) [1]. …”

Section: Introductionmentioning

confidence: 99%

Warfarin Therapy That Results in an International Normalization Ratio above the Therapeutic Range Is Associated with Accelerated Progression of Chronic Kidney Disease

Brodsky¹,

et al. 2010

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Background/Aims: We had previously reported that acute kidney injury (AKI) in warfarin-treated chronic kidney disease (CKD) patients may occur shortly after an acute increase in the International Normalization Ratio (INR) >3.0 with formation of occlusive red blood casts. Recovery from this warfarin-associated AKI is poor. Here we investigated whether excessive warfarin therapy could accelerate the progression of CKD. Methods: We analyzed serum creatinine (SC) and INR in 103 consecutive CKD patients on warfarin therapy in our Nephrology program from 2005 to the present. Results: Forty-nine patients experienced at least 1 episode of INR >3.0. Of these, 18 patients (37%, Group 1) developed an unexplained increase in SC ≧0.3 mg/dl coincident with INR >3.0 (mean SC increase 0.61 ± 0.44 mg/dl); 31 patients (63%, Group 2) showed stable SC (mean SC change 0.04 ± 0.19 mg/dl). Subsequent CKD progression was accelerated in Group 1, but not in Group 2. The 2 groups were not different with respect to demographics, comorbidities, blood pressure, or therapies. However, African Americans were overrepresented in Group 1 (p = 0.035). Conclusions: Overanticoagulation is associated with faster progression of CKD in a high percentage of patients. Our results indicate the need for prospective trials. Nevertheless, we suggest that our findings are sufficiently compelling at this point to justi- fy extra caution in warfarin-treated CKD patients to avoid overanticoagulation.

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Proposed Pathogenesis of Idiopathic Loin Pain–Hematuria Syndrome

Cited by 55 publications

References 27 publications

AKI Associated with Macroscopic Glomerular Hematuria

AKI Associated with Macroscopic Glomerular Hematuria

Pathogenesis of glomerular haematuria

Warfarin Therapy That Results in an International Normalization Ratio above the Therapeutic Range Is Associated with Accelerated Progression of Chronic Kidney Disease

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