Q.312. Mention the contributing factors for development of persistent microalbuminuria & overt Dc. Np.?

DIABETIC NEPHROPATHY 

Revise please the abbreviation list on:

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

Q.311. What are the possible explanations for edema formation given recently? 👌

1)   Capillary H.T.                

2)   Incr. Cpll. Surface area.

3)   Dcr. Cpll. reflection coefficient for pl. proteins .

Q.312. Mention the contributing factors for development of persistent microalbuminuria & overt Dc. Np.?

1)   Poor glycemic control.

2)   Hyperfiltration.

3)   Hypertension.

4)   Smoking.

5)   Retinopathy.

6)   Minimal elevation of urine alb. excretion.

N.B. CKD is a progressive dis.. Kidney dge cannot be reversed, but the condition cn be stabilized. Adequate glycemic control ➤”cornerstone” of diabetes care. Aiming to lower & keep HbA1c < 7 % will result in long-term benefits incl. maintaining kid. function & preventing decline into ESRD. (Medscape).

Q. 313. What is the prognostic factors affecting Dc Np.?

1)   Proteinuria incr. the risk of death 3.5 times comp. to non-diabetics.

2)   Cardiac ANP predicts CVS Morbidity & mortality in Dc Np. I.

3)   Homocysteine 🠝increase CVS Risk in Dc Np. II.

4)   Incr. circululating N-terminal (Probrain) natriuretic peptide: a new independ-ent risk f. of overall & CVS Morbidity/MR in D.M. I & II. é no Sm. of H.F.

5)   Reduction of R. function    CVS Risk.

6)   “Mannose-binding Lectin” & “Symmetric dimethyl arginine” a recent biomarkers for CVS in Dc Np.

Q.314. Mention the putative promoters for prognosis in Dc Np.?

1)   Systemic H.T.

2)   G. H.T. (defective autoregulation é GFR.).

3)   Hyperlipidemia.

4)   Smoking.

5)   Magnitude of proteinuria (>3 g. worse prognosis.).

6)   Dietary protein intake.

7)   Glycemic control (Good impact of tight glycemic control in Dc Np.I. but not in II. Ø delay of progression of DcNp.).

8)   ACE(I.D.)(insertion/deletion) polymorphism: D allele hs deleterious effect é dis. progression.(Losartan, e.g. hs maximum benefit é ACE/DD., comp to I.D. gene).

* N.B.: Non–Dc glomerulopathy is very seldom in proteinuric type I.D.M.., but common in type II. D.M. without retinopathy.

Q.315. Mention the possible extra-renal complication seen in Dc Np?

1)   Dc. Retinopathy, present in All Dc Np.I., but only 50-60 % in Dc Np. II., So abs. of retinopathy requires more investigations for non-Dc G. pathy.

2)   Blindness, due to sev. proliferative retinopathy or maculopathy.

3)   Macroangiopathy: Stroke, carotid stenosis, CHD, PVD: 5 times higher thn non Dc..

4)   P. Np.: in almost all ptn. with advanced Np.

5)   Foot ulcer & sepsis: Ambutation due to combined neural & vascular dis.  

6)   Autonomic Np.: All nephropathic ptn. hv abn. autonomic function tests.

Q316. What are the indications of renal biopsy  👍 in a diabetic 

A. Renal biopsy shd be considered in the foll. situations:

(1) Abs. of Retinopathy in D.M.I., é Prot & R.I. (absense of Prot. doesn’t exclude DN.II.).

(2) Rapid & sudden onset of Prot. esp. in DM.I., its dur.=< 5 Y., or atypical evolution (e.g. N.S. dev. Without microalbuminuria).

(3) Macrohematuria or pres. of active nephritic ur. sediment e.g. acatho-cytosis or RBCs casts, sediment in DM is unremarkable.

(4) Rapid decline in R. func., or R.I. without signif. Prot (first, exclude Renovasc. dis.).

Q317. How to perform a clinical evaluation of D.N.?

A. In diabetic proteinuria u hv to:

1.    Exclude UTI.

2.    Urine microscopy: RBCs, RBCs casts.

3.    Quantitative proteinuria.

4.    Renal U/S.

5.    Serology: ANCA, DNA AB., C3, C4. If GN suspected.

.. Three possibilities will be:    

      Typical DN.: (No Renal biopsy.):

i.             Retinopathy.

ii.            Type I. DM. >10 y.

iii.           Enlarged Kid. on U/S.

iv.           Previous microalbuminuria.

v.            No RBCs Casts.

vi.           No macroscopic hematuria.

      Atypical DN.: (No Renal biopsy.):

1.    Azotemia + proteinuria < 1 g/d.

2.    Papillary necrosis (pyuria, hematuria, scarring.).

3.    Tuberculosis. (Sterile pyuria, hematuria.).

4.    Renovasculer dis. (Other occlusive vascular dis.).

 

      Atypical Prot.:➪ [Renal biopsy.].   †

                                       i.    RBCs Casts.

                                      ii.    No Retinopathy

                                     iii.    Macroscopic hematuria.

                                     iv.    Type I. DM. <10 y.

                                      v.    NRP without progression thr. microaluminuria.

Q.318. What is the broad lines of treatment of Dc Np.?     

1)   Glycemic control: thr. i. Iry prevention. &  ii. 2ry prevention.

2)   B.P. Control: i. 1ry: Before dev. of Dc Np.: Aggressive B.P. control  in normo-tensives to <160/90 in albuminuric Dc II.Ø great reduction of stroke & retinopathy. ii. 2ry prevention: ACEI ØDcr. progression of mico- to macro-albuminuria (2ry), wch. cn be maintained é Normal GFR. for > 8 y.

3)   Lipid Lowering é HMGCoA.

4)   Dietary protein restriction: Low protein diet (0.6-0.8 g/kg/d.): Ø Reduction in UAE & hyperfiltration independent to B.P. & glycemic changes.

Q.319.What options are advisable for Dc ptn commencing ESRD?

A. 1^st 👆option. : R.T.x…. 2^nd & 3^rd Ü H.DX. & P.D. in Equal.   

Q.320. When to start preparation of Dc. Ptn. é Dc Np. for D.X.?

A. Creation of the vasc. access shd be é GFR of👉20-25 ml/min/1.73 m2 .     

Q. 321. When to start D.X.?    ⌚

A. Start of D.X. shd be earlier at a level of GFR of 15 ml/min/1.73 m2, or even earlier é [hyperkalemia, hypervolemia, anorexia or persistent vomiting due uremia or gastroparesis].

Q.322.What specific problems could be seen in dialyzing those patients? What is the explanation?

A. “Intradialytic hypotension”, due to:  ✌

      Disturbance of “counterregulatory” mech., due to autonomic polyneuropathy.    

      Disturbance of L.V. compliance as U.F. dcr. L.V. filling pressure  dcr. C.O.

Q. 323. What is its significance? How to deal with?

A. Intradialytic hypotension cn be complicated by:  

1)   Incr. risk of cardiac death.

2)   Predisposition to myocardial ischemia, arrhythmia & deterioration of maculopathy.

3)   Predisposition to non- thrombotic mesenteric infarction.

** Management: 

1)   Long H.DX. session.

2)   Controlled U.F.

3)   Correction of anemia.

4)   Omit anti-H.T. before D.X.

5)   L- Carnitine Supplementation.

6)   Alternative module e.g. H.F. or CAPD.

Q.324. Give the Optimal renoprotective doses of ARBs?

      Losartan(Diovan) :  100 mg./d.

      Candisartan. (Atacand) : 16 mg/d.

      Irbisartan:  900 mg/d.

  ** N.B. ACEI/ARBs combinationà Reno/Cardioprotection.

Q.325 Mention some famous Trials concerning Dc Np.?

      IRMA study: {The effect of Irbisartan on the development of Diabetic Nephropathy in type II D.M., N Eng J Med 345, 870-878, 2001.}.

      BENEDICT study: {The BErgamo NEphrologic DIabetes Complications Trial, 2003.}.

      EUCLID study: {Randomised placepo-controlled trial of Lisinopril in normotensive patient with insulin-dependent D.M. and normo- or microalbuminuria. Lancet, 349, 1787-1792,1992.}.

Q.326. As a start therapy in H.T./albuminuric ptn é Dc Np. is there is any preference for ACEI vs ARBs.?

A. ADA (The American Dc. Association), recommends  ARBs as initial agent of choice ttt. of H.T. ptn é micro/macroalbuminuria.

Q.327. How can u suspect a diagnosis of “Papillary Necrosis”?

A. D.M. + ✋[UTI+ Septicemia + R. Colic + hematuria + Ob. uropathy]. =    Papillary Necrosis.

Q.328. How can you explain the higher frequency & severity of U.T.I. in D.M.?

1)   Glycosuria 🠞favorable media for growth.

2)   Defective Neutrophil function.                                         

3)   Incr. adherence to uroepithelial cells.

4)   “Detrusor” msc. paresis🠞Impaird evacuation🠞Residual urine é U.B. 

Q. 329. As an option, what is the survival chance for a Dc ptn. in R.Tx. ?

A. Survival in a waiting list = 8 y. .. while in R.Tx. =19 y. Risk of death in R.Tx. in Dc.s = 0.27 comp. to 0.39 in R.Tx. in other glomerulopathies.

Q.330. As a priority in DX., CAPD is superior to other modalities, preferred in DC.s é ESRD, why? 

-  CAPD priority reasons in Dc.s :

1)   Sclerosed forearm vasc. bed for fistula formation & catheterization ( infc. - Poor flow- poor survival).

2)   Better survival (except elderly) comp. to H.DX., if used as initial modality for DX.

3)   Slow sustained U.F., no rapid fluctuation, better B.P.  & U.F. control .

4)   Surgically- wise, No C.I. for R.Tx.

5)   As initial module, then shift to H.DX. (after Kru. decay), hv better survival thn start é H.DX.. Early start é CAPDØ prevents organ dge (owing to term-inal Uremic Insult).

Q.331.What are the main points of interest in this modality?

A. Points of interest:

1)   Wt. gain & calorie gain: the main disadv. (daily absorbed glucose=100-150 mg. /d).

2)   Do Not put insulin in peritoneal bag (! Old fashion)⮞improper dosage, as:

      Insulin binds bag & tubing.                          

      Insulin degraded by insulinase in Pr.                      

      Large individual variation for dose adjustment .

3)   Heat sterilization under a. condition⮞GDPs (highly active Glycosylated Degradation Products): (Glyoxal, methyl Glyoxal, Formaldhyde)Ø AGEP (Advanced Glycation End products), wch. lead to ⮞      Fibrogenesis.

      Neoangiogenesis [due to interaction é RAGE (receptor of AGE)].

      If reached systemic circulationØ Systemic micoinflamm. (Local D.M.).

- Heat sterilization é [Two-comparment bags]= Less toxic (circumvents the generation of GDPs).

Q.332. Comment on glycemic control in Dc.s with R.I.?

A. Glycemic control in R.F. hs two✌opposing mechanisms:

1)   Insulin resistance, (improved by H.DX.).                      

2)   Prolonged ½ life of insulin hypoglycemia, wch. augmented by:                                           i. Anorexia.                                

ii. Accumulation of most sulphonyluria ag.                                                                                     ….. So, use of short acting insulin is advised esp. é surgery & infc.      

.. Most Sulfonyluria hv incr. ½ life, EXCEPT: 

1)   Glimpride (amaryl).     

2)   Gliquidone (Glurenorm.). 

&  Also Non accumulating hypoglycemic drugs:

1.    Glinides.

2.    Glitazones e.g. “Rosglitazone” (Avandia).  

Q.333. What are the recommended drug treatment of diabetes at the various CKD stages? (Comprehensive Medical Nephrology)

A. Drug treatment of diabetes at the various CKD stages:    

   I.        GFR= < 30 ml/min.

1.    Insulin.

2.    Repaglinide. (Novonorm, GlucoNorm; Prandin, Meglitinide Deriv.).

3.    Gliquidone. (Glurenor, Glurenorm, Sulfonylurea).

4.    Rosiglitazone (Avandia.).

5.    No data avalilable for {Sitagliptin, Exenatide, Glimepirid, Gliclazide or Acarbose}.

 II.        GFR= 30-60 ml/min.: The foll. drugs cn be added to I. :

1.    Glimepiride. (Amaryl.).

2.    Gliclazide. (Diamicron.)

3.    Acarbose. (Precose).

III.        GFR= > 60 ml/min.: The foll. drugs cn be added to I. & II. :

1.    Metformin.

2.    Miglitol a (Glyset)

3.    Sitagliptin.  (Januvia 100 mg.).

4.    Exenatide (BYETTA ).

Q.334.What is the role of diuretics in H.T. ptn é Dc Np.?

A. Ptn. é Dc Np. hs a tendency to Salt Retention, So, they’re more prone to Hypervolemia & edema formation  So, [Loop diuretics + Salt restriction ] are advised ….  If the GFR. reached 30-50 ml/min.   “Thiazide” diuretics are useless.     

N.B. Stop diuretics & Rehydrate the ptn. adequately é Saline if a “Radio-contrast” will be applied.

Q. 335. What is the impact of malnutrition on ptn é Dc. Np.?

A. Malnutrition:

1)   A potent independent predictor of “mortality”.

2)   A powerful indicator for “R.R.T.”.

3)    Loss of msc. mass   mis-judge of R.F. severity (Low s. Cr. for low GFR.). ¿ So, use “Cockcroft–Gault” or “Madrid” formula to estimate G.F.R.   

4)   Drug/Dose error.

Q.336.What is the incidence of amputation in Dc.s? & what’s the signif-icance of diabetic foot?

A. 16 % of Dcs undergo amputation due to vascular & neuropathic causes. Diabetic foot is one of the most powerful predictors of survival in dialyzed ptn.,  possibly due to pres. of associated “Micro-inflammatory Status”.