Q.300. Define “Diabetic Nephropathy“?
Diabetic Nephropathy
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
--------------------------------------------------------------------------------
Q.300. Define “Diabetic
Nephropathy“?--
A. A
Clinicopathological syndrome characterized by:
1) Persistent albuminuria (>300 mg/24 h.).
for > 6
m.
2) “Relentless
decline” in GFR.
3)
Raised arterial B.P.
4)
Enhanced C.V.S.
morbidity & mortality.
…. Diagnosed clinically by: ✌
Presence of “Diabetic
Retinopathy”.
Absence of other
evidence of other kidney disease.
It’s the Single 👆 most common
cause of ESRD in Europe, Japan & U.S. (25-45
%) of
all ESRD causes.
Q. 301. What is the hallmark of
Diabetic nephropathy?
A. ➳ [Persistent albuminuria >300
mg/24 h.
or 200 ug/min.].
It is valid for type
I. & II. é 1st
Sn microalbuminuria & 1st Sm odema L.L.
Q. 302. Define Microalbuminuria, what is its significance?
Microalbuminuria =
urinary albumin excretion rate > 30 mg/24h (20 ug/min.) &
< 300 mg /24 h.(200 ug/min), if more.. ➤ macroalbuminuria.
** Significance: 👌
1) Persistent microalbuminuria >
a good predictor of clinical Dc Np.
2) Absence of microalbuminuria >
Lower risk of Dc Np.
3) Incr. incid. of H.T., GFR
decline & other morbid
complications (CVS, CVA).
Q. 303. What are the other medical predictors of
microalbuminuria?
1)
A strong predictor
of total & CVS. morbidity & mortality.
2)
L.V.H.
& Impaired diastolic function.
3)
H.T. & dyslipidemia,
incr. platelet aggregation, endothelial dysfunction.
4)
Incr. insulin
resistance & hyperinsulinemia & autonomic neuropathy.
5)
Marker of widespread
endothelial dysfunction penetration of the
arterial wall by atherogenic lipoprotein plaques.
- Recently, high level
of [N-terminal (Probrain
natriuretic peptide) risk
of C.V.D. in type II. D.M.+ microalbuminuria].
Q. 304. What is meant by Persistant
microalbuminuria?
A. It should be:
Sterile,
non-ketotic.
Micro-range (30-300 mg/24h.) or (20-200 ug/min.).
Two of
three successive sample are +ve .
Q. 305. What are the main physiological
regulators of the GFR?
A. Four F.s :
1) Glomerular plasma flow.
2) Systemic
(oncotic pressure), (plasma proteins).
3) Glomerular
transcapillary hydrostatic pressure difference (not
in human).
4)
G. U.F. coefficient K.F. = product
of hydrolic conduction of G. Cpll. & its S.A..
Q. 306.What is the mean rate of relentless yearly decline in GFR. in Dc Np.?
A. 👉 12 ml/min./y.
Q.307. Give the new
“Pathological” classification of D.M.? 
Glomerulus: shows mesangial expansion: ✌
I.
Isolated
Glomeruler B.M. thickening.
II.
II.a.
(mild) & II.b. (severe): mesangial
expansion.
Diabetic glomerulosclerosis.
III.
<
50 % Glomeruler sclerosis (at least one Kimmlesteil nodule).
IV.
>
50 % Glomeruler sclerosis (Advanced Sclerosis).
Q.308.What pathological changes highly characteristic of Dc Np. I.?
- Capsuler 💧drops
& Subendothelial
Hyaline exudate: 
- “Other diagnostic” changes (in comination):
1) Thickening of G.B.M. (1st
event). *
2) Thickening of tub. B.M.
3) Mesangial expansion (diffuse G. sclerosis).
4) Incr. G. B.M., tub. B.M. & Bowman’s cap. Staining for
IgG.
5) Afferent & Efferent
arterioler hyalinosis. (3-5 y post
D.M.).
6) Kimmelstiel-Wilson Nodules: (Noduler
G.sclerosis, Global G. sclerosis, FSGS, Tub. Sclerosis.).
Q.309. Could Dc Np lesions be reversed?
A. Yes, Reversal of Dc lesions
was recorded after 10 y. of normoglycemia-induced islet
cell of Langerhans T.x.
Reduction of G. B.M., tub. B.M. &
disappearance of kimmelstiel Wilson
Nodules were recorded.
… Suggested mechanism: A Cell-memory process.
Q.310. Enumerate various causes of Nodular Glomerulosclerosis?
1) Idiopathic nodular G.N.
2) Ch.
Membranous proliferative G.N.
3) Dc Np. é Dc
G. sclerosis (Kimmelstiel
Wilson lesion).
4) Dysproteinemia: R. Amyloidosis, M.I.D.D. (Monoclonal
Ig. deposition dis..)
5) Ch. hypoxic & ischemic states: [Congenital cyanotic heart dis.,
cystic fibrosis, Takayasou dis.].
6) Organized G. deposition dis.: Fibrillery & Immunotactoid G.N., Fibronectin G. pathy, Collagen III.
G. pathy.
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
incr.🠝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. delay
of progression of DcNp.).
8) ACE(I.D.)(insertion/deletion) polymorphism: D allele hs deleterious effect é dis. progression.(Losartan, e.g. has 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.
COMMENTS