Cases reported "Hematuria"

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1/29. Acute renal failure in an adult patient with Henoch-Schoenlein purpura after episode of macroscopic hematuria.

    A case of severe prolonged acute renal failure with a histological picture of acute tubulointerstitial lesions in an adult patient with Henoch-Schoenlein purpura after an episode of macroscopic hematuria is described. The macroscopic hematuria lasted only for 5 days and the renal biopsy was performed 50 days after the end of the macroscopic hematuria. Restoration of renal function was not complete six months after the beginning of improvement. Fewer than 65 cases of acute renal failure due to tubulointerstitial nephritis in patients with glomerulonephritis and after episode of macroscopic hematuria have been described in the international literature. Only one of these patients was suffering from Henoch-Schoenlein purpura.
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2/29. Heavy chain deposition disease: the disease spectrum.

    A 45-year-old white woman was found to have microscopic hematuria during her annual physical examination. After a negative urologic workup, she returned 5 months later with nephrotic syndrome, renal insufficiency, and hypocomplementemia. Renal biopsy showed a nodular sclerosing glomerulopathy that could not be further characterized because of inadequate tissue for immunofluorescence. The patient returned 8 months later with chronic renal failure. A repeat renal biopsy showed deposits composed of immunoglobulin g (IgG) heavy chain and complement components C3 and C1 along glomerular, tubular, and vascular basement membranes, with negativity for kappa and lambda light chains, findings consistent with heavy chain deposition disease (HCDD). The heavy chain subclass was exclusively IgG3. Staining with monoclonal antibodies to epitopes of the constant domains of IgG heavy chain showed a CH1 deletion, indicating a truncated heavy chain. On review of the previously reported cases of HCDD, common clinical presentations include nephrotic syndrome, renal insufficiency, hematuria, and, in some cases, hypocomplementemia. In most patients, the hematologic disorder is mild, without overt myeloma. light microscopy shows a nodular sclerosing glomerulopathy, and heavy chain deposits are detectable within basement membranes throughout the kidney by immunofluorescence and electron microscopy. There is no effective treatment for this condition, and virtually all patients progress to chronic renal failure.
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3/29. A child with spider bite and glomerulonephritis: a diagnostic challenge.

    A previously healthy 7-year-old white boy presented to St. Louis Children's Hospital with a 1-day history of headache, malaise, temperature of 38.7 degrees C, and a progressively erythematous, tender calf with central dusky purpura. On the morning of admission, his mother noticed a 2-mm crust on the patient's right calf with a 3-cm x 3-cm area of surrounding erythema. No history of recent trauma or bite was obtained. He had suffered two episodes of nonbloody, nonbilious emesis during the last day. In addition, over the previous 12 h, he presented brown urine without dysuria. His mother and brother had suffered from gastroenteritis over the previous week without bloody diarrhea. On initial physical examination, there was a 6-cm x 11-cm macular tender purpuric plaque with a central punctum on the right inner calf, which was warm and tender to the touch, with erythematous streaking towards the popliteal fossa (Fig. 1). The inguinal area was also erythematous with tender lymphadenopathy and induration, but without fluctuance. Laboratory studies included an elevated white blood cell count of 20, 800/microL with 6% bands, 86% segs, and 7% lymphocytes, hemoglobin of 12.5 g/dL, hematocrit of 35.1%, and platelets of 282,000/microL. The prothrombin time/activated partial tissue thromboplastin was 10. 4/28.0 s (normal PT, 9.3-12.3 s; normal PTT, 21.3-33.7 s) and fibrinogen was 558 mg/dL (normal, 192-379 mg/dL). urinalysis showed 1 protein, 8-10 white blood cells, too numerous to count red blood cells, and no hemoglobinuria. His electrolytes, blood urea nitrogen (BUN), and creatine were normal. The urine culture was negative. Blood culture after 24 h showed one out of two bottles of coagulase negative staphylococcus epidermidis. The patient's physical examination was highly suggestive of a brown recluse spider bite with surrounding purpura. Over the next 2 days, the surrounding rim of erythema expanded. The skin within the plaque cleared and peeled at the periphery. The coagulase negative staphylococci in the blood culture were considered to be a contaminant. cefotaxime and oxacillin were given intravenously. His leg was elevated and cooled with ice packs. The patient's fever resolved within 24 h. The lesion became less erythematous and nontender with decreased warmth and lymphadenopathy. The child was discharged on Duricef for 10 days. Because the patient experienced hematuria rather than hemoglobinuria, nephritis was suggested. In this case, poststreptococcal glomerulonephritis was the most likely cause. His anti-streptolysin-O titer was elevated at 400 U (normal, <200 U) and C3 was 21.4 mg/dL (normal, 83-177 mg/dL). His urine lightened to yellow-brown in color. His blood pressure was normal. Renal ultrasound showed severe left hydronephrosis with cortical atrophy, probably secondary to chronic/congenital ureteropelvic junction obstruction. His right kidney was normal.
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4/29. A case of membranoproliferative glomerulonephritis associated with a hydatidiform mole.

    We treated a 54-year-old woman who was suffering from membranoproliferative glomerulonephritis associated with a complete type of hydatidiform mole. The renal manifestations were proteinuria and hematuria. A renal biopsy, performed before gynecologic management, disclosed focal and segmental subendothelial deposits with a proliferation of the mesangial cell and showed irregularly thickened capillary loops by light and electronmicroscoy. Genralized edema, proteinuria and hematuria were completely recovered by suction and curettage of the hydatidiform mole with prophylactic chemotherapy. The clinical manifestation of earlier presented 3 cases have been the nephrotic syndrome. The common feature of them was a complete remission of the nephropathy after the removal of the hydatidiform mole. The relationship between the hydatidiform mole and glomerulonephritis remains unresolved at present. But we concluded that the hydatidiform mole might be a cause of glomerulonephritis in this case.
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5/29. IgA nephropathy with complement deficiency.

    We treated a female patient suffering from immunoglobulin a (IgA) nephropathy and congenital deficiency of the ninth component of the complement system (C9). She was admitted with hematuria and proteinuria, and the C9 deficiency was diagnosed based on the low hemolytic activity of 50 % of the hemolytic unit of the complements (CH50) and the normal C3 level in the plasma. Renal biopsy revealed mild mesangial proliferation, and immunofluorescence examination revealed mild mesangial deposits of IgA and C3 with the same distribution. We discuss the pathogenesis of IgA nephropathy and the role of the complements in its progression.
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6/29. rhabdomyolysis triggered by an asthmatic attack in a patient with McArdle disease.

    We describe a patient with McArdle disease who developed rhabdomyolysis triggered by a bronchial asthmatic attack. A 64-year-old man had chronic pulmonary emphysema with asthma, and an asthmatic attack led to severe rhabdomyolysis that required continuous hemodiafiltration. After 2 years, a physical examination revealed atrophy of the extremities compared with previous examinations, especially of the intercostal muscles. During that time, he suffered two severe bronchial asthmatic attacks. His serum level of creatinine kinase remained between 4,000 and 7,000 IU/l when he did not suffer from asthmatic attacks and rhabdomyolysis had abated. Therefore, we suspected that his recent muscle atrophy was caused by asthmatic attacks, and discussed the possibility of his respiratory muscle weakness due to McArdle disease in relation to his severe bronchial asthmatic attacks as well as chronic obstructive pulmonary disease.
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7/29. light chain amyloidosis of the urinary bladder. A site restricted deposition of an externally produced immunoglobulin.

    AIMS:To identify the amyloid protein in a patient with amyloidosis localised to the urinary bladder, and to see whether subtyping of the protein by sequence analysis increases the understanding of the selection of the urinary bladder as the site of amyloid deposition. methods:A patient with gross haematuria and a congophilic mass in his urinary bladder was evaluated further. Characterisation of the amyloid protein was performed using conventional histological and immunohistochemical methods. Determination of the N-terminal amino acid sequence of the amyloid protein was performed using protein sequencers. RESULTS:The patient's history, physical examination, and laboratory evaluation excluded the involvement of other organs, justifying a diagnosis of amyloidosis localised to the urinary bladder. Histological and immunological studies showed that the amyloid protein deposited in the urinary bladder of the patient was probably of the amyloid light chain type. No plasma cells or lymphocytes were seen in sections of the urinary bladder and lower ureter adjacent to the amyloid deposits. Molecular analysis showed the sequence NFMLTQPHSISGSPG, which assigned the amyloid protein to either the Vlambda(I) or the Vlambda(VI) immunoglobulin (Ig) light chain families. CONCLUSIONS:The findings suggest that the amyloid protein in this patient originated outside the urinary bladder. The heterogeneity of the Ig proteins in known cases of amyloidosis of the lower urinary tract suggests that the amino acid residues, which determine the Vlambda subtyping, have no major role in restricting the deposited protein to the urinary bladder.
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8/29. A rare case of painless gross hematuria: primary localized AA-type amyloidosis of the urinary bladder.

    A 60-year-old Asian woman presented with a 1-year history of painless gross hematuria. She had no prior urologic history and no other medical problems. Her physical examination, urine cytology, and computed tomography scan were normal. cystoscopy demonstrated several punctate areas of erythema within the bladder. Biopsies revealed amyloidosis, and immunohistochemical staining of the specimens defined the process as amyloid AA (often called secondary amyloidosis). The workup for systemic conditions associated with amyloid AA was negative. This represents an unusual case of primary localized AA-type amyloidosis of the bladder.
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9/29. Intractable bladder tamponade due to left internal pudendal and obturator arterial bleeding induced by erection: a superselective arteriography followed by transcatheter arterial embolization.

    Bladder tamponade is an uncommon clinical symptom among men suffering during sexual intercourse. The authors report on a 46-year-old man for whom this symptom appeared 4-5 years prior to hospitalization. angiography confirmed the presence of left pudendal and obturator arterial bleeding, and embolotherapy of the internal pudendal and obturator arteries was performed. There was no mortality, or limb loss or sexual potency loss at follow-up.
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10/29. hematuria from left internal pudendal and obturator arterial bleeding following sexual intercourse.

    Bladder tamponade is an uncommon clinical symptom among men who experience suffering related to sexual intercourse. The authors report on a 46-year-old man with this symptom 4-5 years before hospitalization. angiography confirmed the presence of left pudendal and obturator arterial bleeding, and embolotherapy of the internal pudendal and obturator arteries was performed. There was no mortality, or limb loss or loss of sexual potency at follow-up.
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