We investigated the relationship of renal lesions with the degrees of proteinuria in 57 type 2 diabetic patients with overt proteinuria (urinary protein excretion rate (UP) > 0.5 g/day) . Creatinine clearance (Ccr) ranged from 25.4 to 131.0 ml/min/l.73 m2. Kidney specimens were obtained and the diagnosis of diabetic nephropathy was made in all patients. The degree of each of the following histologic changes were evaluated:diffuse or nodular lesion, the type of nodular change, mesangiolysis, arteriolar hyalinosis and interstitial damage. We divided the patients into the following 4 groups according to Ccr and UP:group A with Ccr> 60 and UP> 3 g/day (n = 10), group B with Ccr > 60 and UP < 3 g/day (n = 10), group C with Ccr < 60 and UP > 3 g/day (n = 23) and group D with Ccr < 60 and UP < 3 g/day (n = 14), and compared the histologic parameters among the 4 groups. Diffuse index in group A was greater than those in group B (p = 0.05), while those in groups C and D were not different. Nodular index, percentage of patients with nodular lesion did not differ among the 4 groups, however the percentage of glomeruli with complicated nodules (nodular lesion with mesangiolysis and/or microaneurysm) in group C was greater than those in group D (p < 0.05). Hyalinosis index did not differ between group A and B, nor between group C and D, respectively. Interstitial index in group A and B did not differ, however that in group C was greater than in group D (p < 0.05). In addition, the rate of Ccr decrease between renal biopsy and after 12 months was significantly greater in group A and C than in group B and D, respectively (both p < 0.01) . These results suggest that 1) mesangial expansion was associated with the degree of proteinuria in patients with slight impaired renal function, 2) tubulointerstitial involvement was associated with the degree of proteinuria in patients with advanced impaired renal function, and 3) these structural changes might be associated with decrease in renal function in diabetic nephropathy.

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Renal excreted angiotensin converting enzyme (ACE) inhibitor captopril, and renal·hepatic bile excreted ACE inhibitor temocapril, were compared by monitoring serum ACE and renal ACE expression (protein and mRNA) in streptozotocin-induced diabetic rats. Serum ACE levels did not change in untreated diabetic rats or in those treated with temocapril, compared with normal control rats. However, serum ACE levels significantly increased in diabetic rats treated with captopril after 3 months (153.8± 23.0 vs. 43.5±5.5 IU/l/37°C, p< 0.01) and 6 months (113.6± 9.3 vs. 36.9± 2.9 IU/ l/37°C, p< 0.01) compared with normal control rats. Compared with normal control rats (3.6± 0.4), proximal tubular ACE protein expression significantly (p< 0.01) decreased in untreated diabetic rats (1.6 ± 1.1), but significantly (p< 0.01) increased in diabetic rats treated with captopril (3.7± 0.3) and temocapril (3.5± 0.4). Renal ACE mRNA levels decreased in untreated diabetic rats (125.5± 20.3 vs. 313.3± 53.4, p< 0.01) compared with normal control rats for 6 months. Renal ACE mRNA levels tended to increase in diabetic rats treated with captopril (l84.4± 51.2 vs. 125.5± 20.3) and temocapril (165.4± 43.2 vs. 125.5± 20.3) compared with untreated diabetic rats for 6 months. In conclusion, diabetic rats had lower proximal tubular ACE protein expression and lower renal ACE mRNA levels compared with normal control rats. Furthermore, both ACE inhibitors increased renal ACE nrntein and mRNA expressionn but differed in their effect on serum ACE levels.

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We have investigated the clinical characteristics of renal damage and associated complications of 79 patients with accidental hypothermia whom we encountered over the last 5 years. All patients were male, with an average age of 58.9± 9.2 years . Most of these patients were homeless. Body temperature on admission was 29.3± 3.0°C. The most common clinical manifestations on admission were consciousness disturbance and severe hypotension. Complications, including increase in serum transaminase, alcoholism, pneumonia, liver cirrhosis, sepsis, diabetes mellitus, hypoglycemia, acidosis, and an increased level of serum CPK and amylase were found frequently on admission . Death within 48 hours after admission occurred in 23 cases (the death rate;23/79=29 %) . Renal damage was found in 36 cases (36/79=46 %), consisting of acute renal failure (ARF) in 27, and acute on chronic in 6. Urinary diagnostic indices suggested that the etiological factor for ARF was pre-renal, which responded well to passive rewarming and an appropriate fluid replacement therapy, resulting in full recovery in most of the cases (the recovery rate; 25/27=93 %) . Among patients with renal damage, there were no cases requiring dialysis. The present data suggest that accidental hypothermia is a fatal condition with an extremely high deathrate. It also is associated with multiple complications including ARF . The main cause for ARF is prerenal, possibly caused by cold diuresis or dehydration superimposed on the underlying diseases such as alcoholism, diabetes mellitus, liver cirrhosis. Such complications, independent of renal damage, determine the patient's prognosis

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A 22-year-old woman was admitted to our hospital for evaluation of fever, renal dysfunction, and a 3-month-history of macrohematuria . Laboratory evaluation revealed proteinuria (1.8 g/day), hypo proteinemia, microcytic microchromic anemia, renal failure (blood urea nitrogen 30.3 mg/dl, serum creatinine 4.0 mg/dl), and positive serum antiglomerular basement membrane (anti-GBM) antibody . Renal biopsy revealed cellular crescents in all 8 glomeruli and partial rupture of the GBM. The interstitium showed severe inflammatory cell infiltration . Immunofluorescent examination revealed linear deposits of IgG and C3 along the GBM . Pulmonary biopsy revealed linear deposits of IgG along the alveolar basement membrane in the Immunofluorescent examination . A diagnosis of Goodpas ture's syndrome was made because all of the diagnostic criteria were fulfilled . After admission, the patient's renal function deteriorated rapidly . Hemodialysis was started, and the patient was treated with methylprednisolone pulse therapy and oral prednisolone with double filtration plasma pheresis (DFPP) . However, her renal function did not improve. On the 30th hospital day, she showed hemoptysis, and a chest X-ray and CT revealed massive bilateral pulmonary hemorrhage . Despite treatment with pulsed methylprednisolone, oral prednisolone(80 mg/day), and DFPP, the pulmonary hemorrhage improved only transiently, worsening again 5 days later . Cyclophosphamide pulse therapy was administered. After this treatment, the patient's pulmonary manifestations and pulmonary hemorrhage improved. At the present time she is on maintenance dialysis therapy without pulmonary manifestations . These findings suggest that cyclophosphamide pulse therapy is effective against Goodpasture's syndrome with massive pulmonary hemorrhage showing resistance to other conventional therapy .

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We report a case of non-Hodgkin's lymphoma (NHL) presenting with acute renal failure. A-56-year-old male was admitted to our hospital on October, 1997 with fever and renal dysfunction. Physical examination showed no abnormality except for hepatomegaly . Body surface lymphadenopathy was not observed. Computed tomography (CT) of the abdomen showed markedly enlarged kidneys bilaterally and a mass of soft tissue density, which was considered as a swelling lymph node, around the aortic artery. The renal biopsy revealed parenchymal involvement of the NHL cells without normal tubulo-interstitial structure, but the glomeruli were almost intact . Our case rapidly fell into oliguria and acute renal failure, hence needed hemodialysis . After chemotherapy was performed, his renal function gradually improved and the kidney became smaller on subsequent CT. Unfortunately, the patient happened to suffer from methicillin-resistant staphylococcus aureus (MRSA) infection in a neutropenic state and died. Necropsy revealed recovery of the renal interstitium without residual NHL cells . Renal lymphoma without any other organ or nodal involvement is a rare type of NHL, which considered primary renal lymphoma (PRL). However, we believe this case to have been a result of lymphomatous infiltration of the kidneys in disseminated lymphoma .

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Glucosuria was detected in a 7-year-old boy by a routine school mass examination in . The diagnosis of renal glucosuria was made in the affiliated . The patient developed muscle weakness and gait disturbance in . Spinal fluid examination revealed a protein level of 62 mg/dl and a cell count of 4/3. Under the diagnosis of Guillain-Barre syndrome, he was treated with IV immunoglobulin and oral prednisolone. Although the therapy somewhat improved the symptoms, his muscle strength had not fully recovered at the end of the treatment. In the muscle weakness became worse;he could not go up stairs, nor stand upright on one leg. In proteinuria was detected in a school mass examination. He was referred to for a full renal study in Renal biopsy revealed global sclerosis in 16 of 19 glomeruli with extensive interstitial fibrosis and mononuclear cell infiltration. A diagnosis of membranous glomerulonephritis was established based on the findings of spikes in PASM staining, weak IgG deposition in the glomerular capillary and subepithelial deposits by electron microscopic study. Additionally, pituitary growth hormone deficiency was found by endocrinological examination. The diagnosis of CIDP was established by fbulal neuron biopsy, which revealed neuronal degeneration and profound demyelinization. The clinical course of the present case was unlike that of the few reported cases of MGN associated with CIDP described in the literature. The initial renal symptom was glucosuria, which started 5 years prior to the onset of proteinuria. Second, glomerulosclerosis was more extensive than that seen in the literature. We surmise that chronic interstitial nephritis of insidious onset was followed by MGN which developed subsequently, probably at the time of the start of proteinuria.

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