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Expression of endothelial protein C receptor in cortical peritubular capillaries associates with a poor clinical response in lupus nephritis

Izmirly, Peter M; Barisoni, Laura; Buyon, Jill P; Kim, Mimi Y; Rivera, Tania L; Schwartzman, Julie S; Weisstuch, Joseph M; Liu, David T; Bernstein, Stephen; Tseng, Chung-E; Belmont, Howard M; Esmon, Charles T; Merrill, Joan T; Askanase, Anca D; Thomas, David B; Clancy, Robert M
OBJECTIVE: To study the membrane expression of endothelial protein C receptor (mEPCR) in the renal microvasculature in lupus nephritis (LN) as a potential marker of injury and/or prognostic indicator for response to therapy. METHODS: mEPCR expression was analysed by immunohistochemistry in normal kidney and in 59 biopsies from 49 patients with LN. Clinical parameters were assessed at baseline, 6 months and 1 year. RESULTS: mEPCR was expressed in the medulla, arterial endothelium and cortical peritubular capillaries (PTCs) in all biopsies with LN but not in the cortical PTCs of normal kidney. Positive mEPCR staining in >25% of the PTCs was observed in 16/59 biopsies and associated with poor response to therapy. Eleven (84.6%) of 13 patients with positive staining for mEPCR in >25% of the PTCs and follow-up at 6 months did not respond to therapy, compared with 8/28 (28.6%) with mEPCR staining in < or =25% PTCs, P = 0.0018. At 1 year, 10 (83.3%) of 12 patients with positive mEPCR staining in >25% of the PTCs did not respond to therapy (with two progressing to end-stage renal disease) compared with 8/24 (33.3%) with positive staining in < or =25% of the PTCs, P = 0.0116. Although tubulo-interstitial damage (TID) was always accompanied by mEPCR, this endothelial marker was extensively expressed in the absence of TID suggesting that poor response could not be attributed solely to increased TID. mEPCR expression was independent of International Society of Nephrology/Renal Pathology Society class, activity and chronicity indices. CONCLUSION: Increased mEPCR expression in PTCs may represent a novel marker of poor response to therapy for LN
PMCID:2722802
PMID: 19286697
ISSN: 1462-0324
CID: 100419

Comparison of ablative and non-ablative laser treatments of photodamaged skin using objective measurement techniques [Meeting Abstract]

Geronemus, R; Alexiades-Armenakas, M; Feinberg, C; Hawkins, S; Liu, D; Weinkauf, R
ISI:000181880400061
ISSN: 0196-8092
CID: 2144092

B-cell lymphoma presenting as infiltrative renal disease [Case Report]

Mills NE; Goldenberg AS; Liu D; Feiner HD; Gallo G; Gray C; Lustbader I
Acute renal failure is rarely the presenting manifestation of non-Hodgkin's lymphoma. Of the reported cases of renal insufficiency secondary to diffuse renal infiltration with lymphoma, few have presented with acute renal failure. We present a patient with acute renal failure secondary to diffuse bilateral renal infiltration by a B-cell non-Hodgkin's lymphoma. The findings of an elevated serum lactate dehydrogenase (LDH), lymphopenia, and homogenous bilateral renal enlargement on computed tomographic (CT) imaging were important in suggesting the diagnosis of primary renal lymphoma. Renal biopsy with immunohistochemical and ultrastructural analysis was instrumental in confirming this diagnosis
PMID: 1739103
ISSN: 0272-6386
CID: 13695

ROLE OF HYPERPHAGIA IN EXPERIMENTAL DIABETIC NEPHROPATHY [Meeting Abstract]

NEUGARTEN, J; LIU, D; FEINER, H; SCHACHT, RG; BALDWIN, DS
ISI:A1986C539801967
ISSN: 0009-9279
CID: 41403

ROLE OF HYPERPHAGIA IN EXPERIMENTAL DIABETIC NEPHROPATHY [Meeting Abstract]

Neugarten, J; Liu, D; Feiner, H; Schacht, RG; Baldwin, DS
ISI:A1986AXU3600695
ISSN: 0085-2538
CID: 31096

Focal pulmonary edema. Correlation with perfusion lung scan [Case Report]

Tiu S; Liu D; Kramer EL; Sanger JJ
Pulmonary embolism is diagnosed by a mismatched perfusion-ventilation lung scan. The probability is increased further when there is an associated 'hot spot' in the perfusion study caused by focal pulmonary edema
PMID: 4042510
ISSN: 0363-9762
CID: 25924

Nephrotoxic serum nephritis with hypertension: amelioration by antihypertensive therapy

Neugarten J; Kaminetsky B; Feiner H; Schacht RG; Liu DT; Baldwin DS
We have examined the effects of antihypertensive therapy on glomerular dynamics and on the clinical and morphologic features of a model of nephrotoxic serum nephritis (NSN) in which hypertension occurs. NSN was induced in uninephrectomized male Sprague Dawley rats, which drank 0.9% sodium chloride ad libitum. One-half were assigned randomly to a treated group whose blood pressure was normalized on a regimen of reserpine, hydralazine, and hydrochlorothiazide. Hypertension continued throughout the 6 weeks of study in untreated rats (blood pressure 148 +/- 5 vs. 103 +/- 3 mm Hg in treated rats, P less than 0.01). Urinary protein excretion was greater (437 +/- 110 vs. 254 +/- 81 mg/24 hr, P less than 0.005), and serum albumin lower (1.6 +/- 0.4 vs. 2.9 +/- 0.3 g/dl, P less than 0.01) in hypertensive animals. Diffuse glomerular endo- and extracapillary proliferation and arteriolar medial hypertrophy were observed frequently in nephritic rats with untreated hypertension. By contrast, structural abnormalities were limited primarily to focal segmental proliferation involving fewer than one-third of glomeruli in the absence of vascular changes in treated normotensive rats. Micropuncture studies performed 8 to 16 days after induction of nephritis showed a reduction in glomerular capillary pressure (46 +/- 1 vs. 55 +/- 1 mm Hg, P less than 0.001), glomerular plasma flow rate (115 +/- 20 vs. 160 +/- 20 nl/min, P less than 0.01), and single nephron filtration rate (42 +/- 4 vs. 56 +/- 5 nl/min, P less than 0.001) with antihypertensive treatment, suggesting that a hemodynamic mechanism may have been responsible for enhanced glomerular injury in the hypertensive nephritic animals
PMID: 3834224
ISSN: 0085-2538
CID: 65163

AGGRAVATION OF EXPERIMENTAL DIABETIC NEPHROPATHY BY HIGH DIETARY-PROTEIN [Meeting Abstract]

NEUGARTEN, J; LIU, D; FEINER, H; SCHACHT, R; CHUBA, J; BALDWIN, DS
ISI:A1983QL28801650
ISSN: 0009-9279
CID: 40547