Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

LDL-apheresis (LA) was originally used for familial hyperlipidemia, and then in Japan extended to use for the treatment of patients with peripheral arterial disease (PAD) and nephrotic syndrome due to steroid-resistant focal glomerular sclerosis (FGS). The reason why this treatment is applicable for these disorders is due to the fact that LA exerts its favorable effects beyond the lipid-lowering effect. The main underlying mechanisms, for example, in the case of LA application in patients with PAD are: (1) improvement of hemorheology, (2) improvement of endothelial dysfunction, (3) elevations of serum levels of NO and bradykinin, (4) increase in serum levels of vascular endothelial growth factor, and (5) reduction of adhesion molecules on monocytes. Furthermore, we have reported that LA could have anti-inflammatory effects because LA reduces serum levels of P-selectin, which is known to play an important role in the development of atherosclerosis as well as a reduction of serum C-reactive protein levels as standard biomarker of atherosclerosis. Massive proteinuria is also an important challenge in nephrology. The possible mechanisms besides removal of toxic lipids are the reduction of the vasoconstrictive prostanoid and thromboxane A2 (TXA2) and an improvement in macrophage function evidenced by a significant amelioration of interleukin-8 production by lipopolysaccharide-stimulated peripheral blood mononuclear cells. It is intriguing to note that in terms of pharmacodynamics, LA improves steroid and cyclosporine uptake into lymphocytes. Although there are no randomized controlled trials, it is clear that LA has various effects beyond lowering lipids. Making the device more concise and changing it into a whole blood adsorption type, we need to collect more clinical cases and to study the underlying mechanisms further.
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PMID:Applications of LDL-apheresis in nephrology. 1817 56

A 79-year-old woman with familial hyperlipidemia was treated with low-density lipoprotein apheresis. She was hospitalized due to fatigue and edema, and massive proteinuria was discovered. Renal biopsy revealed no distinct abnormalities, thus suggesting a diagnosis of minimal change nephrotic syndrome. She developed acute kidney injury and hemodialysis was initiated. Two series of steroid pulse therapy were given, but the proteinuria did not decrease. Thereafter, she developed thrombocytopenia and fell into a stupor. Thrombotic microangiopathy (TMA) was the most likely diagnosis. Plasma exchange was initiated, resulting in improvements in platelet counts and in her level of consciousness. Clinicians should therefore be aware that TMA can occur as a result of steroid pulse therapy.
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PMID:Thrombotic microangiopathy secondary to steroid pulse therapy administered for refractory nephrotic syndrome. 2404 20