The impacts of COVID-19 on the human kidneys still uncertain. However, experts provide some explanations:
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KIDNEY PROTECTION
Q. How can COVID-19 harm your kidneys?
The impacts of COVID-19 on the human kidneys still uncertain. However, experts provide some explanations:
[1] Coronavirus itself may target renal tissues:
COVID-19 virus itself may infect the cellular components of renal tissues. Renal cell may express multiple receptors that permit coronavirus attaching to these receptors, invading them, and making many copies of itself, therapy damaging renal tissues. Similarly, many receptors elsewhere within the lungs and heart tissues are ubiquitous, where the new coronavirus has been proved to induce injury (AKI).
[2] Hypoxia (deficient oxygen supply) can induce renal dysfunction:
In addition, renal disease in patients with coronavirus can be attributed to an abnormally lowered oxygen concentrations in the blood (hypoxia) that can be attributed to the pneumonia commonly observed in advanced stages of this disease.
[3] Cytokine storm can damage renal tissue:
Our body response to infectious agents may be also contributing. A robust immune response to the new coronavirus can be vigorously triggered in certain individuals that results in a sever cytokine storm when the immune system sends a continuous rush of cytokines into body systems. These cytokines can be observed as minute proteins that assist the cells communicating each other whilst the immune system fighting an infectious episode. However, a sudden rush and a widespread influx of cytokines may induce robust inflammatory response. Whilst fighting to kill the invasive agent, this inflammatory response can damage the healthy tissues, including renal tissues.
[4] COVID-19 can induce blood clotting that block the kidney interior:
Human kidney promotes its function via filtration of toxins, water excess and waste products outside. COVID-19 may induce a very tiny clots formation through the bloodstream that can block the smallest blood vessels in the kidney and impeding its normal function.
Q.51. What
are the indications for RENAL BIOPSYin asymptomatic hematuria/ proteinuria?
A. Mostly, Not necessary, but should
be performed é:
1) GFR. decline.
2) Clinical
suspicion of undiagnosed
systemic dis. aproteinuria, e.g. S.L.E. & M.M.
3) Definitive ttt. depends
on biopsy results.
4) Reassurance of
the ptn. é benign course.
- A.Sm.tc hematuria NOT an absolute indication for biopsy, but some recommend
biopsy é persistent hematuria, esp. é
GFR decline or concomitant
Prot.
Q.52.What laboratory
tests help in diagnosis of glomerulonephritis(G.N.)?
A. Lab.
tests help in diagnosis of G.N.:
1) ANA [ SLE,
esp. é +ve anti-ds DNA A.B or anti-Smith A.B.
2) ANCA [ c-ANCA [ Wegener’s
G.N.
3) P-ANCA
[ M.P.A.
4) Complement [ see Hypocomplementemia Q. No. 10
5) Blood culture [ To
rule out infectious dis. (e.g. Endocarditis).
6) HBV & HCV [ M.N.- M.P.
– Cryoglobulinemia.
7) Cryoglobulinemia [ usually é HCV.
Q.53. Which antihypertensive drugs are SAFE to use in pregnancy? Which drugs are contraindicated?
1) Methyldopa: the
drug most often used in
pregnancy.
2) Hydralazine &
Labetalol:
also effective & safe.
3) Atenolol & diuretics: may be effective, but some
studies ⮞ affect fetal growth.
- On the other hand, ACEI. 🠊 C.I., as they 🠊
1. Neonatal R.F.
2. Congenital malformation.
3. Fetal growth retardation.
Q.54. What is the effect of pregnancy on renal function?
A. By the 2nd
trimester🠊🠉 R.
Pl. flow by 70
% & remain elevated throughout pregnancy. GFR begins to incr. by the
4th
w. of gestation, é peak of 150% at 13 w. & remain elevated until term. So, a S.cr. > 0.9 in pregnancy= R.I. Kidney size enlarge 1-1.5 cm.. Hormonal changes⮞ Ureteric dilatation
⮞ Hydronephrotic picture in U/S. Tub. dysf.
also occurs ⮞Hyperuricosuria, hypouricemia &
glucosuria without
hyperglycemia.
Q.55.What
is the effect of pregnancy on underlying renal disease?
A. Ability to conceive in a
women é R.I. is proportional é degree of R. dysfun-ction. Ptn. us.
exhibits higher
rates of urinary
protein excretion owing to incr. filtration rate (🠉GFR) in pregnancy. The most
important determinant whether R. function deteriorates in pregnancy is 🠊 the level of R.I. At the time of conception. Women é S.cr. > 1.4 mg/dl. at time of conception🠊 is more liable for
decline of R. function. Moreover, underlying R. disease 🠊🠉 Risk of preeclampsia.
Q.56.What
are the renal manifestations of preeclampsia?
A. Preeclampsia: 👉
1) Dcr. GFR.
2) Proteinuria.
3) Glomeruler“Endotheliosis”: Swelling of
the G. endothelial cells.
4) Renal sodium
retention 🠊
edema, ch.ch. this
disorder.
Q.57.What
is the difference between eclampsia & hypertensive encephalopathy?
A. Fundal hallmark of H.T.E.: {Retinal hges, exudates, papillary edema}🠊 rare in eclampsia, wch. ch.ch. by Seizures occ. due to 🠊 cerebral V.C. &
platelet
micro-thrombi.
Q.58. Describe
how does endothelial function deranged in CKD?
A. Endothelial function
derangement is one of the initial steps for atherosclerosis. In Non-renal
ptn., endothelial function us. deranged due to:
1.
H.T.
2.
D.M.
3.
Obesity.
4.
Smoking.
5.
Dyslipidemia.
- In CKD ptn, the following factors are added:
1) Oxidative stress.
2) Insulin resistence.
3) RAAS activation.
4) Reduced activation of vit. D.
5) Reduced intrarenal production of N.O.
6) Low level “persistent inflammation”.
7) Homocysteine & ADMA (Asymmetric
dimethyl-arginine) retention.
8) Reduced production of: EPO, renalase & bone morphogenic protein.
Q.59. Discuss the impact of the aforementioned factors in CVS dis. development ?
1) Oxidative stress: Imbalance
between ROS (Reactive Oxygen Species) & body
ability to inactivate them or repair their dge effect. Despite HOPE (Heart
Out-comes Prevention Evaluation trial) showed: No
benefit of vit. E in 🠊🠉 CVS
risk, some authors still argue: Antioxidants e.g. [vit. E. & acet-ylcysteine]
may be beneficial in CKD.
2) Insulin
resistence & hyperinsulinemia: 🠊🠉 athero.
development, as they present early
in CKD. HOMA technique (homeostatic
model assess-ment) from fasting glc. &
insulin: used to dgx. insulin resistance. HOMA index hs bn used
to predict survival in DX. ptn. Insulin resistance & endothelial dysf.c vsc. dge. ttt.: [Diet, exercise, ACEI, glitazones].
3) Hyperhomocysteinemia:🠉 homocysteine in CKD 🠊🠉 CVS risk. Causes 🠊 multifactorial. But
can be partially corrected by:👉 [vit.B. complex].
4) N.O.
& ADMA: L-arginine – (N.O. synthase) -🠊 N.O. production é vasc.
endothelium. CKD🠊🠉 GFR 🠊 ADMA
retention,
wch’s competitive inhibitor é N.O. synthetase. Incresed ADMA🠊🠉 CKD
progression & increased mortality.
5) Low grade inflammation: Ch. inflammation 🠊 athero.
in CKD & non-CKD ptn. In CKD chronic inflammation🠊🠉 fetuin-A =[Potent
inhibitor of vascular calcification].
6) Abn. bone
mineral metabolism:
(a) Hyperphosphatemia: 🠉 PO4 🠊🠉risk of death in both
early CKD & DX ptn. To dcrease PO4:
both {dietary
restriction+
PO4
binders} :
[Ca.
Carbonate - Ca. acetate- Sevelamer HCL- Lanthanum carbonate] are
needed .
Sevelamer🠊🠉 s. cholesterol & 🠉 risk of progression of
established coronary a. calcification in DX. ptn.
Current recommendation é target s. PO4 (UK.):🠊
Stage 3 & 4 CKD : 0.9-1.5 mmol/L.
D.X. : 1.1-1.8
mmol/L.
(b) Hyperpara.: PTH 🠊 Defective cpll. supply to cardiac myocytes
(animal/ vitro). In ptn.: correction of
sev. hyperpara.🠊
beneficial in calcific uremic arteriopathy.(CUA).
- Effect of correction of
hyperpara. by Cinacalcet
is studied in EVOLVE
study.
- CUA(Calciphylaxis) carries
a v. poor prognosis, é high mortality fr. CVS. dis.
* Risk Factors for
Cardiovascular Disease in Kidney Disease.
Traditional Risk F.s |
|
|
|
Nontraditional Risk F.s |
• Age |
|
|
|
• Kidney function decline
|
FGF-23 = fibroblast growth f. 23. (Kendrick J, et
al.).
Q.60.What
are the insulin & CHO metabolic abnormalities in CKD?
1. Insulin resistence (I.R.).
2. Circulating inhibitors for
insulin action.
3. Dcreased islet cell insulin secretion.
- Insulin
resistance hs bn described in CKD with KRU.
Q.61.What
is the mechanism of insulin resistance in CKD?
A. It is thought to be due to postreceptor abnormalities
induced by:
1) Metabolic acidosis.
2) Lack of Vit.
D.
3) Uremic toxins
accumulation.
4) Proinflammatory cytokines.
5) Others: Uric a., pseudouredine & advanced glycation
end-products.
Q.62.What is the impact of insulin resistance in CKD? How to treat?
A. Insulin Resistence:
1) Endothelial dysfunction, the
early step for athero. development.
2) It
correlate well é CVS mortalities in non-diabetic
DX. ptn.
3) It
contributes to msc. catabolism
DX. ptn.
4) Contribute
to CKD progression via deleterious R. hemodynamic
effects.
*** ttt.: Drugs
that improve I.R.:
1) ACEI.
2) ARBs.
3) 25-(OH.)vit. D.
4) Thiazolidinediones: e.g.
“Generic
Name” |
“Brand Name” |
“Pioglitazone” |
“Actos” |
“Rosiglitazone” |
“Avandia” |
Q.63.What is the impact of dialysis technique on insulin resistance in CKD? How to assess?
A. HDX
& PD. 🠊 partially correct I.R., P.D. hs higher insulinemia
thn HD. & more severe I.R. due to glucose load absorbed fr. glucose-based Dzt
fluids.
- Use of “icodextrin” & a.a. as glucose-free
P.D.🠊🠉I.R. incidence.
- HOMA technique (homeostatic
model assessment) for assessment of I.R.:
HOMA
I.R. calculation:{[Insulin conc. (U U/ml) x
fasting glucose(mmol/L)] / 22.5
}.
Q.64. What is Adipokines?
A. A group of hormones &
cytokines
secreted by adipocytes.The
most important
identified adipokines⮞Leptin & Adiponectin.
- Biological actions of Leptin :
1) Anorexia. 👆
2) Incr. energy
expenditure.
3) Proinflammatory
effects.
4) Proatherogenic
effects.
- Biological actions of Adiponectin :
1) Anti-atherogenic
effect.
2) Anti-inflammatory
effect.
3) Potent insulin-sensitizing
effect.
Q.65.What
is the impact of CRF on Adipokines? Then, what are expected
effects?
A. CRF & ESRDØHyperleptinemia (5-7
times normal & P.D.>
H.D.). & moderate Hyperadiponectinemia
(2 folds rise in
ESRD).
- Factors other thn R. function modulating
hyperleptinemia & hyperadiponectinemia:
1) Fat mass.
2) Acidosis.
3) Inflammation.
4) Hyperinsulinemia.
-Accumulation
of adipokines in CKD augment the decline in R. function thr.:
1) Hyperleptinemia⮞ Protein-energy wasting in
ESRD.
2) Hyperleptinemia ⮞ Worsen sympathetic overactivity
seen in CKD.
3) Hyperleptinemia ⮞ Promotes
H.T.
-Adiponectin : needs
further investigation.
Q.66.What
is the pathogenesis of B2 microglobulinemia?
A. B2M is
a nonglycosylated polypeptide
of 11.8 kDa. It
is a component of the class I major histocompatibility Cx. & present in all
surfaces of virtually all
nucleated cells.
- Clearance by glomerular filtration foll. by proximal tubuler cells uptake
& catabolism.
-Incr. B2M ⮞ A. B2M
formation. Two main causes for incr. B2M:
I. Dcr. clearance:
1) Fall in GFR.
2) DX. modality.
3) Abs. of KRU.
II. Incr. production:
1) Metabolic acidosis.
2) Interferon-a therapy.
3) H.D. membrane bioincombatibility.
4) Lymphoid
cell activation:(clonal
B-cell diso., viral infc., Rhoid arthritis, SLE, Crohn’s).
Q.67. What are antidiabetics that should be avoided in stage III/IV. CKD?
A. For
type II. D.M. & according to K/DOKI guidelines:
1) 1st gen.
Sulphonylurea:[Acetohexamide,
tolbutamide, tolazamide, chlorpro-pamide (é GFR<
50 ml/min) ].
2) 2nd G.S.urea: [Glyburide].
3) Biguanides: [Metformin, avoid: é GFR<40-50 ml/min)].
4) a glucosidase
inhibitors:[Acarbose, miglitol], Not
é
s. Cr >180 umol/l.
Q.68. What oral
antidiabetics that are safe to be used in stage
III/IV. CKD?
A. For type II. D.M. & according to K/DOKI
guidelines:
1) 2ndG.S.urea: [Glipizide & Gliclazide: Nodosa., Glimepiride: Start é 1 mg.].
2) Meglitinides:
[Repaglinide (Novonorm): Nodosa., Nateglinide: Start é 60 mg.].
3) Incretin mimetic: [Exenatide. (Byetta)].
4) Dpp-4 inhibitor:[Sitagliptin:⮞50/75 % é
GFR:< 50/30 ml/min. resp.] .
Q.69. What is the major
criteria of HIVAN (HIV associated nephropathy) ?
A. Major criteria of HIVAN:
1) Higher % of “glomerular collapse”.
2) Severe tubulointerstitial disease .
3) Greater visceral cell swelling.
4) Numerous “tubulo-reticuler” inclusions é G. & vascular endo-thelium.
Q. 70. How can you expect the diagnosis of Rhabdomyolysis?
A. A comatose ptn. é
[msc. tenderness
+ areas of pressure Necrosis +
multiple injuries
+ Bioch.( incr. K+ Po4) + ARF. (Myoglobin Cast ATN.)+
elevated C.K. > 1000 + Normal cardiac “Troponin” & ECG].
= shd. raise the Dg.x. of rhabdomyolysis.
Q. 71. What is the possible therapy in this case?
A. Treatment of “Myoglobin Cast” ATN.,
(Crush Synd.):
1) [Normal
Saline]: one L./h. until urine flow à 20 ml/h. (½ L/d.) à isotonic bicarb., 500 ml/h… do PH..
2) If ptn. is not
oliguric/anuricà [Mannitol] monitor é CVP., k,
Ca balance.
3) H.DX.: intermittent rather CRRT🠊 3 sessions/d. to avoid fatal hyperk.+
** Cautions: 👆 ✌
1. Do NOT use loop diuretics:🠝increase “cast
tubuler Obstruction” & wors-ening of R.F., it has No role in AKI.☜
2. Do NOT
use mannitol in oligo/anuric ptn. (C.I.) .
Q.72. What do you know
about HAN.?
A. Heroin-associated
Np. including:
1) FSGS.
2) Post-infectious G.N.
3) H.B.V.⮞M.N.
4) H.C.V.⮞M.P.
5) 2ry Amyloidosis (multiple skin infection).
6) Interstitial Nephritis.
Q.73. What is “glomerular permiselectivity”? 👆
A. A [property of G. cpll. membrane whereby solutes, including proteins, are restricted fr. passage across cpll. wall into⮞ urinary space]. Exclusion of a protein fr. Bowman’s space is based to some extent on its molecular size & conformation, but mostly fr. its net Negative charge. Negatively charged proteins are excluded fr. G.U.F due to their inability to pass thr. Negatively charged endothelial cells. تنافر G. cpll. B.M. are surrounding endothelial cells & epithelial structures that comprise the slit diaphragm.
Q.74. What
is “functional proteinuria” (F.P.)?
A. [Transient protein excretion ass.:
fever, strenuous exercise, emotional
stress & CHF]. One explanation
is🠝 R.B.F. 🠊🠉 albumin
excretion, the other: H.F. & Renovscular H.T. 🠊🠉 Angio.II 🠊proteinuria, due to Direct effect of Angio.II.
on G. Permiselectivity.
Q.75. Define
“asymptomatic proteinuria”(A.Sm.tc
Pr.)?
A. Urine excr. us. range fr. 40-80 mg/d., but most labs define 150 mg/d. = upper limit of normal. A.Sm.tc proteinuria= {urinery
protein excretion >150
mg/d, but
<3.5 g./ d., but No ass. Sm or Sn of N.S.
(odema,
hypoalbuminemia, hyperlipid-emia, thrombotic comp.}. Ptn us. excr.< one
g./d.
A.Sm.tc Pr. ass. é less
serious consequence than those é N.S.
Q.76.What
are the most common causes of asymptomatic
proteinuria” (A.Sm.tc Pr.)?
A. A.Sm.tc Pr. either G.
or tub. diso. (NRP.
usually G.), G. proteinuria aexcr. of high m.w. proteins e.g. albumin
& globulin,
where as tub. proteinuria
a smaller protein as well.
** “Glomerular”
causes:
1) Functional proteinuria.
2) Orthostatic proteinuria.
3) Early glomerular dis.
** “Tubular” causes”:
1) A.T.N.
2) Pyelonephritis.
3) Analgesic nephopathy.
4) Ch. K+ depletion.
5) Overflow proteinuria.
6) Heavy metal intoxication.(Cadmium).
7) Hereditary (Fanconi Synd., Wilson’s dis.).
Q.77. What
is “orthostatic”proteinuria
(Postural proteinuria)? What
is overflow proteinuria (overproduction)?
A.“Orthostatic”proteinuria : [a
condition é wch. ptn. excrete excess ur. protein only é upright position]. It occ.
almost always é young
men &
us.< one g./24 h., é No ass. G. lesion
& é spontaneous resolution é 5-10
y. Dgx.:Elevated
daytime(morning to bedtime: 16 h.)+ Normal night (to morning=8 h.) ur. protein. If
both collection are high a persistent
proteinuria.
- overflow proteinuria: A
clinical condition: conc. of filtered protein exceeds tubuler reabsorptive
capacity, occurs usually é paraproteinemias,
e.g. M. myeloma, monoclonal gammopathy., or
light chain dis. Alth. mechanism is us. overflow, subsequent
G. proteinuria cn occ. due to G. defect.
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