Erythrocytosis Associated With the Nephrotic Syndrome

Sonneborn, Robert E.; Pérez, Guido O.; Epstein, Murray; Martelo, Orlando J.; Pardo, Victoriano

doi:10.1001/archinte.1977.03630200070019

Cited by 15 publications

(4 citation statements)

References 22 publications

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“…True polycythemia is an unusual event in association with nephrotic syndrome and its pathogenesis remains unclear. To our knowledge, this association has only been described in adult nephrotic patients with glomerulosclerosis, chronic glomerulonephritis, or membranous glomerulopathy (Table 1) [1,2,3,4]. In our patient, the clinical course as well as the association of extremely high renin activity with low-normal erythropoietin levels indicates that polycythemia was spurious rather than true, although an isotopic study to exclude increased red blood cell mass was not performed.…”

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confidence: 70%

Severe acute abdominal pain in a patient with steroid-sensitive idiopathic nephrotic syndrome

Amil

Santos

Ordoñez

et al. 2002

Pediatric Nephrology

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Keywords Severe acute abdominal pain · Steroid-sensitive idiopathic nephrotic syndrome Sirs, A 14-year-old white male was admitted to our hospital because of severe abdominal pain of acute onset. No diarrhea or vomiting had been noted. Eleven years before he had been diagnosed with steroid-sensitive idiopathic nephrotic syndrome. He had presented with 14 relapses, the last 19 months prior to admission. No medication other than prednisone had ever been used to induce remission of proteinuria. In an attempt to avoid relapses, the boy had been placed on prophylactic treatment with 5 mg of oral prednisone every other morning for the last 6 months. Because of the steroid sensitivity, a renal biopsy had not been performed. The family history was negative for renal diseases and polycythemia.Physical examination revealed minimal palpebral edema, diffuse abdominal pain without signs of peritoneal inflammation, normal chest auscultation, and good peripheral circulation. His weight was 68.5 kg. Blood pressure was 100/55 mmHg. Laboratory tests showed blood hemoglobin 20.5 g/dl, hematocrit 62.2%, white blood cell count 33,100/µl, platelet count 443,000/µl, serum albumin 13.5 g/l, serum total proteins 35.5 g/l, serum sodium 128 mEq/l, serum urea 82 mg/dl, serum creatinine 1.4 mg/dl, cholesterol 359 mg/dl, serum triglycerides 296 mg/dl, and serum osmolality 285 mosmol/kg. Activated partial thromboplastin time (32.3 s), prothrombin time (11.7 s), and levels of plasma fibrinogen (534 mg/dl) were within normal ranges. Urinalysis revealed proteinuria, microhematuria, and granular casts. Urinary volume (24-h) was 620 ml (15.5 ml/m 2 per hour), creatinine clearance 119 ml/min per 1.73 m 2 , natriuresis 2 mEq/l, protein/creatinine ratio 7.9 mg/mg, and urine osmolality 899 mosmol/kg. His peripheral plasma renin activity was 95.4 ng/ml per hour (supine) (reference values 1.3-4 ng/ml per hour) and serum erythropoietin concentration was 8.6 mU/ml (reference values 5-25.2 mU/ml). Doppler ultrasonography of inferior cava and renal veins was normal. On admission, treatment was started with 80 mg/day of i.v. methylprednisolone followed by 80 mg/day of oral prednisone, 200 mg/day of oral aspirin, 40 mg/day of subcutaneous low molecular weight heparin, and ranitidine 50 mg t.i.d. i.v. for 3 days and thereafter 150 mg b.i.d. by the oral route. On the 3rd day of admission, the patient was free of symptoms, his weight was 67.5 kg, proteinuria had decreased, and blood hemoglobin was 17.5 g/dl. He was discharged on the 5th day of admission. During follow-up, proteinuria became negative and hemoglobin returned to normal values of 12.8 g/dl.The highly elevated concentrations of hemoglobin and hematocrit found in the patient presented here are rarely observed in patients with nephrotic syndrome, even during the first episode of nephrotic syndrome when the time elapsing from the appearance of proteinuria until a correct diagnosis is made is usually much longer than that required to identify the relapses. Hypovolemia and hemoconcentration, consistent wit...

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confidence: 70%

Severe acute abdominal pain in a patient with steroid-sensitive idiopathic nephrotic syndrome

Amil

Santos

Ordoñez

et al. 2002

Pediatric Nephrology

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“…Polycythemia is seldom seen in patients with MN, renal hypoxemia due to severe nephrosis leading to increased EPO production is the main stimulus. The etiology for polycythemia in chronic kidney diseases proposed were as follows: increased EPO production due to renal hypoxia, increased sensitivity to EPO, and abnormal feedback regulation of erythrocytosis [16][17][18][19]. The increased activity of renin-angiotensin system was involved in this process, and the beneficial effect of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type I receptor blockers in control of polycythemia after renal transplantation was the basis for this [18,19].…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Membranous Glomerulonephritis Leading to Secondary Polycythemia: A Rare Association

Yadav¹,

Pathak²,

Malik³

2023

Cureus

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Primary polycythemia is caused due to mutations in erythropoietin (EPO) receptor or Janus Kinase 2 (JAK2). Secondary polycythemia is seldom associated with renal diseases, such as adult polycystic kidney disease, kidney tumors (like renal cell carcinoma and reninoma), renal artery stenosis, and kidney transplant due to increased EPO production. Polycythemia associated with nephrotic syndrome (NS) is very rare. Here, we report a case with membranous nephropathy, the patient had polycythemia at presentation. Nephrotic range proteinuria causes nephrosarca leading to renal hypoxia which causes increased EPO and IL-8 production, this is proposed to cause secondary polycythemia in NS. The reduction of polycythemia following remission in proteinuria further suggests the correlation. The exact mechanism remains to be found out.

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“…Two adults cases with nephrotic syndrome and polycythemia were found. [5,6] However, no infants or children were found with this association. Polycythemia does seem possible with nephrotic syndrome due to hemoconcentration caused by hypoproteinemia and edema.…”

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confidence: 89%

Vomiting in a Neonate

2011

IJPN

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At 22 days of life, a girl presented with one day of vomiting after every feed. The vomit was milk colored, without bile or blood. Since birth, she had intermittent vomiting. She had no diarrhea, cough, congestion or fever. Her urine output was decreased. Case and diagnonis are discussed in the case report. CASE At 22 days of life, a girl presented with one day of vomiting after every feed. The vomit was milk colored, without bile or blood. Since birth, she had intermittent vomiting. She had no diarrhea, cough, congestion or fever. Her urine output was decreased. Also, her parents felt that her eyelids were puffy.

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Erythrocytosis Associated With the Nephrotic Syndrome

Cited by 15 publications

References 22 publications

Severe acute abdominal pain in a patient with steroid-sensitive idiopathic nephrotic syndrome

Severe acute abdominal pain in a patient with steroid-sensitive idiopathic nephrotic syndrome

Idiopathic Membranous Glomerulonephritis Leading to Secondary Polycythemia: A Rare Association

Vomiting in a Neonate

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