Liver ultrastructural and biochemical changes in the prenephrotic stage of aminonucleoside nephrosis

Lewin, Peter K.; Moscarello, Mario A.

doi:10.1016/0014-4800(68)90003-8

Cited by 14 publications

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In fact, CF VIII and AIII decreased. The mechanism by which this happens is unknown, yet these alterations may be related to the direct toxic effect of PAN on the liver [43] instead of the nephrotic condition itself. Fig.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Cruz

Juárez-Nicolás

Tapia

et al. 1994

Nephron

View full text Add to dashboard Cite

The human nephrotic syndrome is accompanied by important alterations of the coagulation system related proteins. The purpose of the present study was to examine the activity of coagulation- and fibrinolysis-related proteins in plasma and urine of control and puromycin aminonucleoside injected rats on days 2 (prenephrotic stage) and 10 (nephrotic stage). We measured the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the activities of (1) the coagulation factors (CFs) I, II, V, and VII-XII; (2) the inhibitor of coagulation antithrombin III (ATIII), and (3) the component of the fibrinolytic system α₂-antiplasmin (α₂-APL). PT and aPTT and the activities of CF, ATIII, and α₂-APL were not measurable in the urine of control and puromycin aminonucleoside injected rats on day 2. On this same day, plasma ATIII and CF VIII decreased. On day 10 (1) PT and aPTT decreased in plasma and were not measurable in urine; (2), plasma CFs I, II, V, VII, VIII, X, and XI increased; (3), plasma ATIII decreased; (4), plasma CFs IX and XII and α₂-APL did not change, and (5) ATIII and CFs II, VII, VIII, IX, X, XI, and XII, but not CFs I and V and α₂-APL, appeared in urine on day 10. ATIII deficiency was secondary probably to the urinary losses; however, the plasma activity of CFs II, VII, VIII, X, and XI increased and that of CFs IX and XII remained unchanged in spite of their urinary losses which suggests that other mechanisms such as deranged catabolism and altered hepatic synthesis may be involved. This model may be useful to study the pathophysiology of the abnormalities of coagulation in humans with nephrotic syndrome.

show abstract

Section: Discussionmentioning

confidence: 99%

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Cruz

Juárez-Nicolás

Tapia

et al. 1994

Nephron

View full text Add to dashboard Cite

show abstract

Effects of renal factors on in vitro hepatic cholesterol synthesis in the rat

Haven

Jacobi

1971

Lipids

View full text Add to dashboard Cite

Two products derived from rat renal tissue have been shown to affect in vitro hepatic cholesterol synthesis. A premevalonate inhibitor of hepatic cholesterol synthesis is associated with the membranes of the renal endoplasmic reticulum. It is stable at −75 C and at 4 C but is heat labile. A pre‐mevalonate stimulator of in vitro hepatic cholesterol synthesis is located within renal lysosomes and can be prepared in a nonsedimentable form by extraction with hypotonic buffer. While it is stable at −75 C, it loses activity at 4 C. Both of these products appear to have a molecular weight in excess of 150,000 as determined by gel filtration.

show abstract