Lipoprotein (a)[Lp (a)] is an independent risk factor for cardiovascular disease. The level of Lp (a) is markedly elevated in end-stage renal disease, particularly in patients with diabetic nephropathy. In the present study, the morphological distribution of apo (a) and scavenger receptors within the arterial wall are described. Autopsy specimens of the left coronary artery and the thoracic aorta were examined immunohistochemically. Lp (a) accumulates in the intima in proportion to the serum Lp (a) levels. Most of the Lp (a) was located in the intima of the arterial wall. A strong co-localization of apo (a) and scavenger receptors was found. We conclude from these data that modified Lp (a) is taken up, in part, by macrophage scavenger receptors, trasforming them into foam cells. This leads to further progression of atherosclerosis in patients with diabetic nephropathy and chronic renal disease.

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Glomerular clearance (GC), tubular reabsorption (TR) of albumin and the relatioship between TR and tubular load of albumin were assessed in 108 patients with NIDDM without proteinuria (I; AER≤15, II; 15-49.9, III; 50.0-199.9μg/min) and in 31 healthy controls to clarify the relative contribution of GC and TR to AER. GC and TR of albumin were determined by inhibiting TR of albumin using L-arginine infusion.
In controls and NIDDM-I, AER was significantly correlated with GC of albumin, while no correlation existed between them in NIDDM-II and III. No significant difference in GC of albumin was found in relation to the degree of microalbuminuria. On the other hand, AER in 3 groups of NIDDM increased in close relation with deterioration of TR of albumin. Furthermore, when TR of albumin was plotted against the tubular load of albumin, there was a linear relationship between them in all subject groups. The regression lines in controls and NIDDM-I were quite similar, while within the tested range of tubular load, the capacity of TR deteriorated in relation to the advance of microalbuminuria.
These results indicate that in a state of normal AER, TR as well as GC of albumin determine AER, and that the reduced TR of albumin plays a causal role in the development of microalbuminuria in NIDDM.

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This study aimed to identify potential risk factors for diabetic neuropathy. The frequency of neuropathy and its association with clinical findings were examined in 1212 non-insulin-dependent diabetics during their initial visit to the Third Department of Internal Medicine, Tokyo University. Neuropathy was defined as the presence of symptoms consistent with distal polyneuropathy, or the absence of tendon reflexes.
The overall prevalence of neuropathy was 28 %, with no difference between the sexes. It increased with the duration of diabetes. Neuropathy was found to be associated with age, duration of diabetes, maximal body mass index, body mass index (inverse), symptoms at the time of diagnosis, prior diabetes treatment, and fasting and post-load plasma glucose levels. Family history, alcohol consumption, smoking, blood pressure and cholestrol level were not associated with the occurrence of neuropathy. Multivariate analysis showed that fasting plasma glucose levels (x²=40.1) and duration of diabetes (x²=40.0) are statistically significant risk factors for neuropathy.
The results of this study indicate that the frequency of neuropathy is extremely high in diabetics, and that hyperglycemia and duration of diabetes are strongly related with the development of neuropathy.

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We have used the ¹³³Xe clearance method to measure peripheral perfusion pressure (PPP) and peripheral resistance (PR) in order to study the effect of Lipo PGE₁ on peripheral circulation in diabetic patients. The subjects consisted of 50normal subjects and 21 DM patients with a history of at least five years. The PPP and PR of the DM subjects were significantly lower than those of the normal subjects. However, administration of Lipo PGE₁ caused a significant increase in the PPP and PR of these subjects. Impairment of peripheral circulation in DM patient is reportedly caused by ASO and continuous dilation of the arterio-venous shunt vessels, thereby resulting in a steal phenomenon of blood. Our examination revealed that Lipo PGE₁ takes effect selectively only in vessels more central than arterioles, to increase PPP and PR, and is thus effective in improving impairment of peripheral cirulation in DM patients.

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We report the case of a 48 year-old woman. At the age of 38 years, she was diagnosed as having diabetes mellitus. Three years later, she became aware of orthostatic hypotension, residual urine and palpitations, but there were no abnormal findings on routine tests. Subsequently, a 3243 mitochondrial tRNA (leu) mutation was documented in her leukocytes, and myocardial imaging using ¹²³I-labeled beta-methyl-iodophenyl pentadecansic acid (¹²³I-BMIPP) revealed abnormal uptake in the lateral, inferior, and apical myocardium. These abnormalities resolved after coenzyme Q₁₀ therapy.
This suggested that the ¹²³I-BMIPP test might be useful in detecting subclinical cardiac abnormalities associated with this mitochondrial mutation, and might be capable of being used to confirm the effects of Coenzyme Q₁₀ therapy. Furthermore, it can be inferred that vasomotor dysfunction may have induced her various autonomic symptoms.
We conclude that in view of the circulatory dysfunction due to the mitochondrial abnormality caution is warranted when diagnosing mitochondrial diabetes mellitus patients with various autonomic symptoms.

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A 29-yar-old man with the nephrotic syndrome presented with fasting hypoglycemia (40-50mg/dl) and hyperinsulinemia during treatment with prednisolone. Daily profiles of plasma glucose and insulin, and a 75 g oral glucose tolerance test revealed mildly abnormal glucose tolerance and hyperinsulinemia. A C-peptide suppression test showed that the C-peptide level was reduced from 3.3 to 1.2ng/ml. An abdominal CT examination revealed diffuse enlargement of the pancreas without any abdominal mass. The fasting plasma glucose level increased to normal as the dose of prednisolone was decreased. No symptoms of hypoglycemia have been observed during the 8-year follow-up period. The fasting glucose and insulin levels remain normal. Therefore, the fasting hypoglycemia with hyperinsulinemia in this case was probably caused by treatment with prednisolone.

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A 37-year-old woman with insulin-dependent diabetes mellitus had been on insulin therapy (32 unit/day). She had cold on 5 February 1993, and stopped insulin injection because of nausea and dyspnea. On 10 February, she was admitted to our hospital because of progressive dyspnea. Her consciousness was clear, body temperature 37.7°C, respiratory rate 32/minute, blood pressure normal and dehydration mild. Plasma glucose was 501 was mg/dl, metabolic acidosis was present (PaO₂ 99.7 mmHg), WBC was 18400/mm³, and CRP was 20 mg/dl. No abnormal findings were found on chest X-ray and electrocardiogram. TAT and D-dimer were already increased on admission. We made a diagnosis of diabetic ketoacidosis and started intravenous insulin infusion and fluid replacement immediately. Although hyperglycemia and metabolic acidosis improved, dyspnea became worse, and hypoxia and leukopenia developed rapidly. Diffuse infiltrative shadows appeared in the chest X-ray with reduction in the platelet count 12 hours after treatment. We made a diagnosis of ARDS and DIC. Although treatment by mechanical ventilation with positive end expiratory pressure and Nafamostat was given, she died 35 hours after admission. Autopsy proved marked pulmonary edema compatible with ARDS, and bronchopneumonia with microabscesses caused by Staphylococus aureus. This is a rare case of diabetic ketoacidosis complicated with rapid progression of ARDS, DIC, and Leukopenia. It apperas that, in addition to infection, injury of the pulmonary capillaries and hypercoagulability and DIC related to her diabetic state and acidosis might have precipitated ARDS with the consequence of intrapulmonary sequestration of leukocytes.

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