What are the renal toxic manifestations of antiviral therapy? How to manage?
CLINICAL NEPHROLOGY
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?
A. [R.F.
+ H.T. + Gout = ⮞Lead 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.? 👍
(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