Nefropatías Diabéticas Flashcards

1
Q

Microalbuminuria

A
  • Normal 100-300 mg albúmina / día
  • marcador de daño renal y un testigo de nefropatía diabética precoz.
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2
Q

Síntomas de nefropatía diabética

A

Aumento de excreción de albúmina y proteína en la orina

Aumento de la presión arterial

Descenso de la función renal

Asociado a

Mayor riesgo de enferemdades cardiovasculares

Retinopatía diabética

Neuropatía diabética

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3
Q

Compromiso Renal de la Nefropatía Diabética Etapa I

A

Hipertrofia renal;

Hiperfiltración (Cl creatinina de 140-160 ml/min)

Aumento del volumen glomerular y renal

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4
Q

Compromiso Renal de la Nefropatía Diabética Etapa II

A

Lesión renal sin signos clínicos
Aumento del grosor de la membrana basal
Aumento del mesangio celular
Hiperfiltración aun sin proteinuria
Evoluciona en años

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5
Q

Compromiso Renal de la Nefropatía Diabética Etapa III

A

Nefropatía Incipiente
Microalbuminuria persistente
Alteración del Heparán Sulfato y proteoglicanos por glicosilación lo que produce desnaturalización de la membrana basal
Esclerosis del mesangio
HTA clínica

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6
Q

Compromiso Renal de la Nefropatía Diabética Etapa IV

A

Nefropatía establecida
Proteinuria >300 mg/dl, aquí se llega al Síndrome nefrótico
Caída de la filtración glomerular de ± 10-12 ml/min/año
Hipertensión arterial más elevada
Retinopatía diabética

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7
Q

Compromiso Renal de la Nefropatía Diabética Etapa V

A
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8
Q

HISTOPATOLOGIAde la Nefropatía Diabética

A

Finalmente,esta expansión mesangial puede conducir a dos diferentes patterns morfológicos:

Glomeruloesclerosis Nodular : marcada por una acumulación nodular de matriz mesangial (lesiones de Kimmelsteil- Wilson ) o bien,

Glomeruloesclerosis Difusa: caracterizada por aumento difuso de la matriz mesangial.
Otros hallazgos alM.L. incluyen depósitos de fibrina, engrosamiento de la membrana basal tubular, esclerosis hialina arteriolar, y engrosamiento de la íntima arterial.
Al M.Electrónico se observan engrosamiento de la membrana basal, hiperplasia de la matiz mesangial,gotitas ded lípidos, depósitos de complejos no-inmunes

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9
Q

Efectos del factor de transformación- de crecimiento beta (TGF-ß),

A

TGF-b: es una citoquina hipertrófica y proescle- rótica considerada el principal factor etiológico de la nefropatía diabética

ha demostrado ser mediadora en casi todos los cambios morfológicos de la nefropatía diabética.

Este factor de crecimiento es responsable de la producción excesiva de matriz extracelular en las células glomerulares y tubulares, y su

síntesis es estimulada por los valores elevados de glicemia plasmática.

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10
Q

Efectos de la hiperglicemia

A

Hyperglycemia may also induce multiple
adverse effects indirectly through activation and formation of metabolic end molecules such
as oxidative and glycation products and by activation of protein kinase C (PKC), transforming
growth factor beta (TGF-b), and the renin-angiotensin system.

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11
Q

Advanced glycosylated end products (AGEs)

A

formed from the nonenzymatic reactive binding (glycation) of sugar-derived carbonyl groups with a reactive amino group resulting in formation of an unstable Schiff base with subsequent Amadori rearrangement to form a more stable ketoamine.

In cultured glomerular endothelial and mesangial cells, in vitro, glycated albumin, and AGE-rich proteins enhance expression of type IV collagen and TGF-b and increase PKC activity,

contributing to glomerular sclerosis and tubulointerstitial damage by means of an abnormal
 extracellular matrix (ECM) production.
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12
Q

TGF-b

A
  • TGF-b modulates ECM production in glomerular, mesangial, and epithelial
  • cells.
  • inhibits synthesis of collagenase
  • stimulates the production of
  • metalloproteinase inhibitors, which could lead to reduced degradation of ECM
  • In renal biopsies from diabetic persons with nephropathy, increased TGF-b immunostaining has been described both in glomeruli and the tubulointerstitium.

Increased renal production of TGF-b and increased urinary TGF-b levels, findings noted in patients with
type 2 diabetes, as correlates of urinary albumin excretion (UAE).

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13
Q

PKC

A
  • Hyperglycemia is the predominant stimulus that induces activation of distinct PKC isoforms within a cell, each mediating specific functions probably via different subcellular localization.
  • PKC activation increases production of cytokines and extracellular
    matrix and vasoconstrictor endothelin-1
  • These changes contribute to basement membrane
    thickening, vascular occlusion, and increased cell membrane permeability
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