Lung tissue from 9 patients dying in different stages of an acute respiratory distress syndrome due to septicemia was fixed by a postmortem transthoracic injection method for an ultrastructural and morphometric analysis. At the initial stage of septic lung disease a widespread interstitial and alveolar edema was the essential finding. The capillary endothelium was relatively well preserved; in particular, no large endothelial gaps could be detected. In contrast, local destruction of the squamous epithelium, often covered by hyaline membranes, and a rapid proliferation of Type II epithelial cells were noted. In the subacute stage, cuboidal transformation of the epithelium and fibrotic alterations of the interstitium were the predominant findings. The extent of fibrotic alterations of lung architecture was not clearly related to the time course of the disease; on the other hand, the thickening of the air-blood barrier estimated by morphometry mirrored the disturbances of gas exchange and lung mechanics. The nonspecificity of the lesions observed in the subacute as well as in the acute stage of the disease provided further evidence of a uniform and characteristic reaction pattern of the lung that does not reflect the type and route (via blood or inspired air) of the damaging agents. Hence, it appears questionable whether lung biopsy specimens obtained from patients with acute respiratory distress syndrome can contribute to the diagnosis of the underlying disease.
Glomerular hyperfiltration, which is expected to occur after uninephrectomy, could potentially damage the non-transplanted donor kidney in living donor transplantation. We therefore prospectively measured renal function (inulin and PAH clearance), albumin excretion and blood pressure in the donors of 30 consecutive living donor kidney transplants before uninephrectomy (n = 29) and 1 week (n = 27) and 1 year (n = 16) after. Hyperfiltration was defined as: (post-nephrectomy inulin clearance )/(0.5 x pre-nephrectomy inulin clearance); hyperperfusion was defined in an analogous way for PAH clearance. Hyperfiltration averaged 128 ± 5% [SEM] and hyperperfusion 133 ± 6% 1 week after uninephrectomy. Hyperfiltration was nearly unchanged (126 ± 7%) 1 year after nephrectomy, whereas hyperperfusion had significantlydecreased to 118 ± 8% (P < 0.02). There was no significant change in blood pressure after nephrectomy, and no new cases of hypertension were observed during the 1-year follow-up. The degree of hyperfiltration did not correlate with donor age. Microalbuminuria > 30 mg/24 h was found in two donors 1 week after nephrectomy (one of which normalized at 1 year) and in one additional donor 1 year after nephrectomy. The degree of hyperfiltration did not correlate with albumin excretion rate. In conclusion, no adverse consequences of hyperfiltration were demonstrable during the 1-year observation period, but the prognostic role of occasional microalbuminuria should be further investigated.An increased glomerular filtration rate, also termed 'hyperfiltration' is considered an important factor in the pathogenesis of various nephropathies and in the non-immunological progression of chronic renal failure [4]. The paradigmatic example for this is the hyperfiltration which Offprint requests to:
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