Q.235. What is calcific uremic arteriopathy (CUA)?

 

KIDNEY PROTECTION

Revise please the abbreviation list on:

https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372

 

?Q.235. What is calcific uremic arteriopathy (CUA  

A. CUA= Calciphlaxis: Ch.Ch. by diffuse medial calcification of the small & medium-sized arterioles. Intimal proliferation & thrombosis occ. Painful skin ulceration & necrosis. Parathyroidectomy (Pec.) may be beneficial if there’s marked hyperpara. Warfarin ppt. the syndrome, probably by f.VII-depend-ent anticoagulant proteins.

?Q.236. What’s Calciphylaxis? What is new in its therapy

A. Caciphylaxisis a: {Systemic “medial calcification”, in ESRD ptn. é sev. Hyperpara. ttted é Vit. D.}. D.D.: [Cellulitis- vasculitis- mixed Cryo.- cho-lesterol embolization]…       New therapies include:

      Hyperparic O2 therapy.

      “Pamidronate” & oral “etidronate” Ü resolve ulcers & calciphylaxis les.

?Q.237. Describe the evolution of MIA syndrome

A. Malnutrition, Inflammation & Atherosclerosis synd. describes wasting as part of an inflmm. state ass. é CVS dis. It's not responsive to édietary intake. MIA explains the é CVS risk é failing kidney. The evolution of athero. is an inflmm. process, é é evidence that CRP enhances this proceass. CKD ptn haveé CRP & other proinflmm. cytokines incl. IL-6. The low s. albumin sn in MIA reflects ongoing inflammation &Feffect of cytokines on GIT, rather poor nutritional intake. ®

?Q.238. How could “sickle cell” anemia harm the kidney

A. Sickel cell Nephropathy incl. the foll.:[ Gross hematuria-Renal infarct-papillary necrosis.- N.S.- Medullary carcinoma & inability to conc. urine.] FSGS is the most common cause of renal failure in sickle cell anemia.

 ?(Q.239. Define Hepatorenal syndrome (HRS

A. HRS: [Unexplained ARF in the context of severe hepatic dysfunction]. Oliguria present é 90% of cases, low B.P., jaundice, ascites & metabolic encephalopathy: (Somnolence + Confusion + Astrexis) are common finding. Two types were recognized:

v    Type I HRS Ø Rapid decline in GFR, defined as: doubling of s.Cr.>2.5 mg/dl or 50 % reduction in Cr.Cl. to <20 ml/min. within 2 weeks.

v    Type II HRS Ø hv more prolonged course & better üprognosis.

?Q.240. What is the pathogenesis of HRS

A. Arterial V.D. in splanchnic circulation, triggered by portal H.T., play a central role in hemodynamic changes & decline in R. function in cirrhosis . Mech.: incr. V.D. activity & production (mainly splanchnic circulation), é N.O. is most important. As hepatic dis progress Ø rise in C.O. & fall in systemic vsc. resistance occ.; the latter change occ. despite local increments in R. & femoral vascular resistance tht result in part fr. Hpt-induced activation of renin-angiotensin & S.N.S.. So, dcr. in total vasc. resistance must occ. in splanchnic circulation, under influence of N.O. derived fr. the endothelium. Bacterial translocation fr. intestine into mesenteric lymph nodes play an important role in this process.

Decline in R. perfusion is ass. é reductions in GFR & Na+ excretion (<10 meq /d. in sev. cirrhosis) & fall in mean arterial B.P., despite intense R.V.C.. Importance of splanchnic V.D. in these changes cn be illustrated by the resp. to ornipressin (ADH analog) tht’s a preferential splanchnic V.C.. In Ptn. é advanced cirrhosis: ornipressin & vasopressin analogues partially corrects many of systemic & R. hemodynamic abn. wch. incl. rise in mean arterial B.P., reductions in pl. renin activity & norepinephrine & incr. in RBF, G.F.R. & ur. Na+ excretion & volume. Response to portasystemic shunt also supports the importance of splanchnic hemodynamics in HRS genesis. Portasystemic shunting hs improved R. function in a limited No. of ptns. although it’s not currently used as ttt. for this disorder.

“Summery”:

Actual cause: Unclear, but imbalance betw. systemic V.D. & R. V.C. Ø Under-filled “arterial vasculature” + R.V.C.Ø R. hypoperfusion. Sugg. vasoactive ag.:

I. Candidate systemic V.D.: [N.O.- atrial natriuretic peptide- intestinal bacterial endotoxin, substance B & false neurotransmitters (Octopamine, Phenoethanolamine)].

II. Candidate renal V.C.:[Endothelin, catecholamines, Angio.II., low bradykinine, éV.C. PG, êV.D. PG]. A constellation of several factors hs bn postulated.

Q.241. What are the suggested relation between cancer incidence and both Iry renal disease and ongoing therapy?

A. I. Cancer &“Iry”R. dis.:

1)   Von Hipple-Lindau dis.Ø

auto. dom. familial cancerØ[ multiple benign & 

malignat tumors:Kid., adrenals, CNS & pancreas].

2)   Analgesic Nephropathy ØTransitional cell carcinoma.

3)   Balkan Np. ØTransitional cell carcinoma .

  II. “Cancer & ttt. of R. dis.”:

1)   Cph.Øéincidence of neoplasia (cancer U.B.), appear decades later.

2)   Im/m. é CKD & ESRDØ é risk of cancer.

3)   R.Tx.: certain cancers are more common: non-melanoma “skin” cancer, Post Tx. Lymphoprolifertive diso.

4)   Risk of neoplasia is linked to reg. used, é mTOR inhibitors e.g. rapamycin<Ø Antiproliferative effect & ê risk of neoplasia.