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CLINICAL NEPHROLOGY

What are the renal toxic manifestations of antiviral therapy? How to manage?

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CLINICAL NEPHROLOGY

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:

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

Q. How can acute kidney injury (AKI) complicate COVID-19 infection?

Early reports (Wuhan) denotes that almost 3-9% of hospitalized COVID-19 infected patients may develop AKI. This percentage, however, have been jumped to 15% of hospitalized subjects and almost 20% or more in ICU-admitted patients where dialysis therapy may be commenced. Furthermore, AKI can be considered a clinical marker of COVID-19 intensity that can be associated with a high mortality. Many COVID-19-related factors have been implicated in AKI development:

1)   Enhanced blood clotting,

2)   Microinflammatory processes,

3)   Directly infected renal tissues.

4)   Renal tubular injury (ATN) with associated sepsis,

The post-COVID-19-related AKI period is characterized by a lowered kidney function after discharge.

 

Q127. What are the renal toxic manifestations of antiviral therapy? How to manage?

A. Renal toxicity of antiviral therapy:

   I.        “Protease” inhibitors:

1.    Indinavir:🠊 {Crystalluria-Nephrolithiasis-Dysuria- AKI- I.N.}. ttt.🠊 Daily fluid intake>2 L/d. N.B. Ritonavir & Lopinavir:🠝 indinavir toxicity.

2.    Ritonavir:🠊 {Reversible AKI, us. in combination é nephrotoxic drugs}.

3.    Saquinavir & Nelfinavir:🠊{Renal calculi, rare}. ttt.🠊 🠝 fluid intake.

 II.        Reverse Transcriptase inhibitors:

1.    Tenofovir, abacavir: 🠊 {Renal tub. dge: proximal tub. dysf., Fanconi synd., Nephrogenic D.I., ATN, AKI}. ttt. 🠊 Pt. on tenovir: monitor Sn of tub. dysf.:[🠝 S. Cr., HypoPo4,🠋 S. uric a., glucosuria, Prot. & acidosis.].

2.    Didanosine, Lamivudine, Stavudine:🠊{Tub. dysfunction.}.

III.        Others: Cidofovir, adefovir:🠊 {R. tub. dge, proximal tub. dysf. (cidovir)}.

 

Q.128. What recommendations should be applied with Methotrexate prescription in CKD patients?

A. Methotrexate:

Not é GFR < 50 ml/min./1.73 m2.

Not é TMP/SMX 🠞 severe pancytopenia.

Folic a. 5 mg. B.D. should be added.

- Dose: 0.3  mg/kg/w., max, 15  mg/w.

Q.129. What are the general indications of infliximab?

A. Infliximab: (Remicade 100 mg.) is a monoclonal chimeric Anti-TNFa blocker, used é the foll. indications:

(1) Wegener’s granulomatosus.

(2) Sarcoid  kidney.  , .. Other medical indications:

(3) Chronic inflamm. bowl dis.( U.C. & Crohn’s dis.).

(4) Rhomatoid arthritis.

(5) Psoriatic arthritis & Plaque.

- Other TNFa : Etanercept (Enprel) 50 mg/w.

Q.130. When can you expect the Dgx. of Lead Nephropathy?    

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A. [R.F. + H.T. + GoutLead Np.]. Although hyperurecemia is common in R.F., Gout is unusual, but if present, shd raise the possibility of  Lead Np.

Q.131. Enumerate the different types of renal disease in S.L.E.?   👍

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(1) Abnormal urinalysis (hematuria and/or proteinuria) with or without  🠉 Pl. cr. observed in up to 75 % of ptn. The most frequent  abnormality is proteinuria.

(2) Classification system (2004) 6 diff. G. dis. classes (biopsy guided):

Class I: (minimal mesangial): msng. immune deps. identified either by I.F. alone, or by I.F. & E/M., but without L.M. abn. Class I. hs N. urinalysis & s. cr..

Class II(mesangial prolif.):L.M.: Msng. hypercellularity & matrix expan-sion.I.F. & E/M:few isolated subepith. or subendoth. deposits, but no subendoth. depos. seen on L.M. Ptns present é microscopic hematuria and/or proteinuria; H.T. is uncommon & N.S. & R.I. virtually never sn.

C. III: (focal Prolif.)L.M.: endo- or extracpll. G.N. é < 50 % of G.. Focal sub-endothial depos. on E/M. It’s further subdivided acc. to chronicity. Hematuria & proteinuria sn in almost all ptns, some hv N.S., H.T., and/or 🠉Pl. cr.. Progr. R.I.: uncommon if< 25% of G. affected &G.: segmental prolif. without necrosis.

Class IV (diffuse Prolif.):>50 % of G. hv endocpll. é or without extracpll. G.N.. Class IV. subdided into segmental (IV-S) & global (IV-G) dep. on G. hv segm-ental or global les., resp..Subclasses depend on chronicity. Hematuria & proteinuria occ. in all ptns é active dis., & N.S., H.T., R.I. are frequently observed.

Class V (membranous L.N.): L.M: diffuse thickening of G. Cpll. wall. I.F or E/M: subepith. immune depos.. Alth. subendothelial depos.  cn be sn by I.F or E/M alone, such depos. detected by L.M need combined Dgx. of C.III/IV.&V .. N.S. us. sn., alth. hematuria & H.T. may be sn., Pl. cr. us. N. or mildly raised.

C.VI (adv. sclerosing):global sclerosis é >90 % of G. It represents healing of prior inflmm. inj., & advanced stage of ch. C.III, IV, or V. L.N.. Ptns display slowly progr. R. dysf. + proteinuria & relatively bland urine sediment.

(3) Tub. interstitial dis. occ. é G. dis. & may be the only manifestaion of L.N.. Ptn.s present é rising pl. cr.+ bland urinalysis. Sn of tub. dysf. may be present.

(4) Vascular dis.: common and cn affect the prognosis of R. dis.. Ptns may present é G. & vasc. thrombi, often + aPL A.B.(e.g. LA & anticardiolipin A.B.).

(5)Silent L.N.: Msng., focal, or diffuse prolif. G.N. No clinical dis.(us. benign).

(6)Drugs: lupus-like synd., esp. those acetylated in liver, [e.g. hydralazine, procainamide & INH.]. R. dis.: uncommon but prolif. G.N. or N.S. cn occur.


Q.132. How to treat diffuse or focal proliferative lupus nephritis?

A. Clinical risk f. for progression:[🠉 S. cr. at  time of R. biopsy, H.T., NRP, anemia, blacks or Hispanics & on R. biopsy: crescents & sev. tub. interstitial dis.]. Prompt Dgx. & therapy🠞 clinical remission of active disease🠞 improved long-term prognosis. Non-im/m. therapy: given to almost all ptns é prolif. L.N., even those requiring im/m..  Persistent Prot: ACEI/ARBs, initiate monothp. & target minimum dcr. in Prot. 🠞 60 % from baseline é goal of < 500-1000 mg/d. Goal B.P.< 130/80 mmHg. Thpy directed also to dyslipidemia & hypercoagulability é N.S.

Im/m. thp. for proliferative L.N consists of induction & maintenance:

Induction: involves im/m. drugs to achieve clinical remission; delayed initiation of such thp & failure to attain clinical remission 🠞 worse outcomes.

v  Focal prolif.:(=<25 % of G. affected on L.M. + no necrotiz les. or crescent form., N. B.P. & s. cr., & Non-NRP): trial of Steroids alone:60 mg. /d./one w., taper. to 30 mg/E.O.D./total3m. Goals of thp 🠞 loss of hematuria &🠋 Prot. Ptns not resp. or progress: ttted as if they hv diffuse proliferative LN.

v  Moderate/Sev. focal prolif. or diffuse prolif. LN.🠞 im/m. thpy: [Steroids + either i.v. Cph or oral MMF]. Choice depends upon clinical features (e.g, “MMF” prefered in blacks & Hispanics) and ptn preference (e.g., young woman want to avoid ovarian toxicity of Cph). We recomm.:i.v. Cph in more sev. dis. (e.g., elev. s. cr. and/or crescents on R. biopsy) .

-If i.v. Cph is chosen 🠞 short course regimen is recommended .                                     

- If MMF is chosen 🠞 ALMS trial:[MMF comp. é Aza. ws ass. é statistically & clinicl signif. dcr. in relapse rate in  ALMS maintenance Trial & nonsignificant trend toward benefit in MAINTAIN nephritis trial. ]  «ألَمَظ» Sev. active dis. (eg, ARF, florid crescentic  G.N., sev. extrarenal dis.) 🠞 Sterods initiated é i.v. Mprd (500-1000 mg/30 min./d./3d.)🠞 rapid im/m. effect since resp. to i.v. Cph  is not seen for 10-14 d. .  (هام جداً)

 

Q.133. What about maintenance therapy of diffuse or focal proliferative L.N.?

A. {Ptns completed induction therapy& attained remission maintenance im/m. for at least 18-24 m. or longer . { سنَتِين}. 

 Aza. or MMF are recommended over Cph for maintenance, it depends upon  initial induction therapy:

Ptns received i.v. Cph 🠊 Aza; 2 mg/kg/d. max. 150-200 mg/d.. Don’t start Aza until WBCs => 4000 cells/microL& absolute neutrophil =>1500 cells/microL, then