Negative pressure wound therapy for prolonged surgical wound healing after brachiobasilic arteriovenous fistula creation in a patient with end-stage liver failure.

A 54-year-old male patient diagnosed with hepatorenal syndrome caused by decompensated alcoholic cirrhosis was referred for arteriovenous fistula (AVF) creation after initiation of hemodialysis. A brachiobasilic arteriovenous fistula (BBAVF) was created because neither forearm had suitable vasculature. Large-volume serous effusion from the incision persisted postoperatively, and we started negative pressure wound therapy (NPWT) for wound protection. The effusion volume decreased gradually; however, up to 80 ml of discharge continued daily. Re-operation was performed 35 days after the initial operation, followed by continued NPWT. The wound was almost healed 85 days after the primary surgery. We present a case of severe surgical wound complication after AVF creation in a patient with hemostatic and coagulation disorders and malnutrition caused by end-stage hepatic failure. We confirmed the usefulness of NPWT for excessive surgical wound effusion and the adequacy of BBAVF for vascular access.

[Case of microscopic polyangiitis accompanied by central nervous system symptoms and brain vasculitis observed histopathologically].

A 65-year-old-man complained of coughing and fever. The urine showed microscopic hematuria. The level of myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) was 167 EU. Two months later, he was admitted to our hospital with pulmonary hemorrhage and progressive renal dysfunction. He was treated with intravenous methylprednisolone followed by oral prednisolone with plasma exchanges, and his first pulmonary hemorrhage was relieved. Three weeks later, he suffered from a second diffuse pulmonary hemorrhage with central nervous system symptoms. He was treated again with intravenous methylprednisolone, plasma exchanges, and also intravenous pulse cyclophosphamide (IVCY), but he died of respiratory failure. Autopsy findings revealed microscopic polyangiitis (MPA)in the brain as well as in the lung, kidney and gastrointestinal system. The histopathological findings suggested that cerebral nervous system symptoms could have been caused by brain vasculitis in this case.

Cerebral microvascular disease predicts renal failure in type 2 diabetes.

Abnormalities in small renal vessels may increase the risk of developing impaired renal function, but methods to assess these vessels are extremely limited. We hypothesized that the presence of small vessel disease in the brain, which manifests as silent cerebral infarction (SCI), may predict the progression of kidney disease in patients with type 2 diabetes. We recruited 608 patients with type 2 diabetes without apparent cerebrovascular or cardiovascular disease or overt nephropathy and followed them for a mean of 7.5 years. At baseline, 177 of 608 patients had SCI, diagnosed by cerebral magnetic resonance imaging. The risk for the primary outcome of ESRD or death was significantly higher for patients with SCI than for patients without SCI [hazard ratio, 2.44; 95% confidence interval (CI) 1.36 to 4.38]. The risk for the secondary renal end point of any dialysis or doubling of the serum creatinine concentration was also significantly higher for patients with SCI (hazard ratio, 4.79; 95% CI 2.72 to 8.46). The estimated GFR declined more in patients with SCI than in those without SCI; however, the presence of SCI did not increase the risk for progression of albuminuria. In conclusion, independent of microalbuminuria, cerebral microvascular disease predicted renal morbidity among patients with type 2 diabetes.

[Cerebral salt wasting syndrome in a patient with viral meningoencephalitis].

A 53-year-old male was admitted to our hospital for a high fever. He suffered a change in personality, memory loss and disorientation as well. The findings of cerebrospinal fluid showed monocytosis, but the titers of glucose, C1 and ADA were all normal. Although there was no bacterium in the CSF, the patient's electroencephalography finding was abnormal. We diagnosed his condition as viral meningoencephalitis and started treatment with antiviral agents. Blood chemistry showed serum sodium of 130 mEq/l and plasma osmolarity was reduced to 272 mOsm/kg, while urine osmolarity was high at 353 mOsm/kg. Two potential causes of hyponatremia in this patient were the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting syndrome (CSWS). Physical findings revealed a contracted extracellular fluid volume, strongly suggesting the presence of CSWS. The massive urine sodium loss overcoming sodium intake supported this diagnosis. After treatment with vigorous sodium and volume replacement for over 4 weeks, hyponatremia as well as meningoencephalitis were improved without any complication. To the best of our knowledge, this is the first report on CSWS in a patient with viral meningoencephalitis.

ANCA-negative pauci-immune crescentic glomerulonephritis complicated with recurrent massive gastrointestinal hemorrhage.

On April 25, 2003, a 62-year-old Japanese man had been admitted to a hospital because of heavy proteinuria and elevated serum creatinine level, and purpura on the lower extremities. On May 15, 2003, he was referred to our hospital for evaluation and treatment. Serum immunoglobulin and complements were within normal ranges. Immune serology was negative for antinuclear antibody, antiglomerular basement membrane antibody, and antineutrophil cytoplasmic antibodies. Histological examination of a percutaneous renal biopsy specimen revealed that all of the glomeruli had severe crescent formation without deposits of immunoreactants. A diagnosis of antineutrophil cytoplasmic antibody-negative pauci-immune crescentic glomerulonephritis was made. The patient was treated with one cycle of steroid pulse therapy (1000 mg methylprednisolone daily, given on 3 consecutive days), and subsequently with prednisolone (60 mg/day). Despite this treatment, renal failure progressed rapidly and hemodialysis was started 1 month after the acute presentation. On May 30, 2003, he suddenly developed massive hematochezia. A technetium-targeted red-blood-cell scan suggested bleeding in the small intestine. On June 11, he presented with massive melena. A bleeding ulcer was found in the third part of the duodenum, and was treated successfully with endoscopy, using a heater probe. On June 19, he presented with massive hematochezia again. Mesenteric angiography revealed active bleeding from the iliac branch of the superior mesenteric artery. He was treated with continuous intraarterial vasopressin infusion by a catheter seated in the branch artery. The majority of patients with pauci-immune crescentic glomerulonephritis, one of the most common causes of rapidly progressive glomerulonephritis, have glomerular disease as part of a systemic vasculitis. Massive gastrointestinal bleeding, although rare, should be considered one of the serious complications in these patients.

Thiazide diuretics enhance nocturnal blood pressure fall and reduce proteinuria in immunoglobulin A nephropathy treated with angiotensin II modulators.

OBJECTIVE: We examined whether thiazide diuretics could restore nocturnal blood pressure (BP) decline and reduce urinary protein excretion in patients with glomerulopathy treated with angiotensin II modulators (angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers). METHODS: Twenty-five Japanese outpatients (11 men, 14 women; mean age 43 +/- 12 years) with biopsy-proven immunoglobulin (Ig)A nephropathy, preserved renal function (serum creatinine concentration

Effect of corticosteroid therapy on the progression of IgA nephropathy with moderate proteinuria.

BACKGROUND: In patients with heavy proteinuria, corticosteroid therapy has been shown to have favorable effects on the progression of IgA nephropathy. However, the efficacy of corticosteroids on the progression of IgA nephropathy with moderate proteinuria is still controversial. METHODS: We assessed 45 adult (age, 18-50 years) patients with moderate proteinuria (0.5-2.0 g daily) and preserved renal function, (serum creatinine concentration, < or = 106 micromol/l) who were diagnosed as having primary IgA nephropathy between December 1993 and July 1998. Twenty-three of the patients were treated with corticosteroids (steroid group), and the remaining 22 patients had no steroid treatment (control group). All patients were followed up for more than 3 years. RESULTS: There were no differences in baseline characteristics between the two groups, except for proteinuria. In the steroid group, urinary protein excretion was significantly higher than that in the control group. During the follow-up period, urinary protein excretion was not changed in the control group. On the other hand, in the steroid group, mean urinary protein excretion decreased significantly. Seven patients in the control group and 2 patients in the steroid group reached the endpoint, which was defined as a 50% increase in serum creatinine concentration from baseline. Renal survival curves were significantly different between the two groups. A second biopsy was performed in 20 patients who received steroid therapy. Mesangial cell proliferation, mesangial matrix increase, and cellular crescents were significantly reduced in the second compared with the first biopsy specimens. CONCLUSIONS: Steroid therapy is effective in reducing the progression of IgA nephropathy with moderate proteinuria.

[Two cases of lupus cystitis complicated by lupus nephritis treated successfully with steroid therapy].

In patients with systemic lupus erythematosus(SLE), interstitial cystitis(lupus cystitis) is an uncommon, but important manifestation. We report two Japanese patients with lupus cystitis. Case 1 was a 49-year-old woman diagnosed as having rheumatoid arthritis and membranous nephropathy. She was treated with prednisolone(5 mg daily). Case 2 was a 41-year-old woman also diagnosed as having rheumatoid arthritis previously and treated with a non-steroidal anti-inflammatory drug. Both cases presented abdominal pain, vomiting, dysuria and frequency of micturition. We diagnosed these cases as SLE on the basis of arthritis, renal disorder(proteinuria and hematuria), and positive antinuclear and anti-dsDNA antibodies. In addition, bilateral hydronephrosis was found in both cases. Thus, they were also diagnosed as probable lupus cystitis. The patients were treated with one cycle of methylprednisolone pulse therapy. Thereafter they were treated with 60 mg/day of prednisolone and their symptoms resolved promptly. Furthermore, no abnormal finding was found by abdominal ultrasonography and/or the intravenous pyelogram after therapy. Renal biopsies were performed and both cases showed lupus glomerulopathy (case 1: WHO class Vb, case II: WHO class IVb). Abdominal pain and/or dysuria, which is common in SLE patients, requires further examinations to evaluate the lupus cystitis.

Clinical course of bucillamine-induced nephropathy in patients with rheumatoid arthritis.

BACKGROUND: Bucillamine, a disease-modifying antirheumatic drug widely prescribed in Japan, is reported to be a cause of proteinuria. However, to date, the clinical course of the nephropathy associated with the use of bucillamine has not been described in detail. METHODS: We analyzed renal biopsy findings from 10 patients with rheumatoid arthritis and concomitant bucillamine-induced nephropathy. Each patient was followed up until proteinuria had resolved. RESULTS: Proteinuria appeared 2-11 months after the initiation of the treatment with bucillamine. Nine patients, who stopped bucillamine treatment immediately (within 3 months) after the onset of proteinuria, were diagnosed as having stage I membranous nephropathy. Only one patient, who used bucillamine for 9.5 months after the onset of proteinuria, was diagnosed as having stage II membranous nephropathy. In all patients with stage I membranous nephropathy, the proteinuria disappeared within 7 months after they stopped bucillamine treatment. On the other hand, in the patient with stage II membranous nephropathy, the proteinuria persisted for 14 months after the use of bucillamine was stopped. In all the patients, the proteinuria resolved completely without deterioration of renal function. None of the patients has experienced recurrence of proteinuria. CONCLUSIONS: In patients with proteinuria induced by treatment with bucillamine, membranous nephropathy is the most common disorder. Immediate withdrawal of bucillamine results in prompt and complete resolution of proteinuria without deterioration of renal function.Bucillamine, a disease-modifying antirheumatic drug widely prescribed in Japan, is reported to be a cause of proteinuria. However, to date, the clinical course of the nephropathy associated with the use of bucillamine has not been described in detail.