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Q.221. What is the hallmark lab. of TTP-HUS?


renoprotective meaning renoprotective antihypertensive drugs renoprotective ace inhibitors renoprotective antidiabetic drugs renoprotective agents renoprotective arbs renoprotective antihypertensive renoprotective action

Revise please the abbreviation list on:


Q.221. What is the hallmark lab. of TTP-HUS?    ✋

 A.    Hallmark lab. of TTP-HUS: (Microangiopathic hemolytic anemia):

*                  LDH.

*                  Retics.

*                  Indirect Bilirubin.

*                  Low Haptoglobin.

Q.222. How to D.D. DIC. from TMA?

 A. TMA has Normal: (PT, PTT, Fibrinogen level & Coagulation profile).

Q.223. How to ttt. refractory TTP-HUS?

A. Ptns é: 

1)   Relapsing dis.,or

2)   Severe course who don’t rapidly respond to Pph, or

3)   Worsen é neurologic abnormal despite (Pph + steroids), we recommend:

                     ✌   [Rituximab or Csp + Pph twice/d.].

Q.224. What are the criteria of good & poor prognosis?

A. Good prognosis”:   😃😃

          *      Young Age.

*      Summer diarrhea.

*      Early Dgx. & ttt.

Poor prognosis”:    😌😌

      Older children.

      Winter cold months diarrhea.




      Need for DX.

      Severe vascular lesion é R. “Biopsy”.


Q.225. How can you diagnose R.A. occlusion (thrombosis)?


A. RAT: [Hematuria + loin pain + LDH. +anuria]. (contralateral reflex spasm).

- The gold standard in Dgx. 👉Angiography.

N.B. Radiographic evaluation of peripheral a. or coronary a. disease often reveals that R.A. lesion are also present (ie, incidentally discovered RAS). Such ptn. do not require therapy directed at R. vasculature since there’s evidence that R.A. revascularization does not improve B.P., R. function, or other outcomes in this setting.   

Q.226. For how long can the kidney afford absence of blood? ⌚⌚

A. Our Kidney can tolerate abs. of blood (e.g. R.A.T.) for 60-90 min. ( h. maximum).

Q.227. What are the most common coagulation disorder in nephrotic syndrome?

A.Two principle” mechanisms are responsible: 

       I.        Activation of G. hemostatic mech.:intraglomeruler thrombin formation”.

     II.        Urinary loss of:  

(1) Antithrombin III.

(2) Plasminogen.

(3) a2-antiplasmin

(4) Free protein S.

-    N.B.: Hypoalbuminemia:

1)   Platelet hyperaggrigability.

2)   Alteration in fibrinolytic system.

3)   Procoagulation proteins.

Q.228. What is the most common complication of atherosclerosis, and what is the most common organ involved ?

A. H.T. is the most common complication of atherosclerosis, and Kidney is the most common organ involved in autopsy.

Q.229. What is the most common extrarenal complication of atherosclerosis? What is its significance?

A.Cutaneous” manifestations, it heralds Renal involvement.

Q230. What is the role of APOL1 in evolution of early renal dis. in African Americans?

A.Two separate dis. -causing polymorphisms in apolipoprotein L1 (APOL1) gene found exclusively in African Americans, inherited as autosomal recessive traits confer a higher risk of ESRD. In addition, APOL1mutations are ass. é earlier on-set of kid. dis.. Study: 407 African Americans receiving HDX, ptn. é two mutant alleles were signif. younger at time of DX initiation thn those without any dis.-causing APOL1 mutation (49 vs 62 y.). In a large population based study incl. 1776 African Americans without known kid. dis. (mean age 45 y.s), homozygotes for APOL1 mutations were more likely to hv microalbuminuria (18 vs 9 %) & estimat-ed GFR < 60 mL/ min per1.73 m2 (6 vs 3 %) comp. é other individuals.

Q.231. Explain how is the incidence of vascular calcification increased in CKD?