Nefropatia diabetica
Introduzione
La nefropatia diabetica è la causa principale di insufficienza renale cronica. E’ una delle cause principali di morbilità e mortalità correlate al diabete mellito di tipo I e di tipo 2. La proteinuria nei soggetti con DM è associata a marcata riduzione della sopravvivenza e aumento di rischio di malattia cardiovascolare. Gli individui con nefropatia diabetica quasi sempre hanno anche retinopatia diabetica. Come le altre complicanze microvascolari, la patogenesi della nefropatia diabetica è correlata a iperglicemia cronica. I meccanismi attraverso i quali l’iperglicemia cronica determina la malattia renale, anche se non completamente definiti, sono i seguenti:
- interazione di fattori solubili (fattori di crescita, angiotensina II, endotelina)
- alterazioni emodinamiche nel microcircolo renale (iperfiltrazione glomerulare)
- modificazioni strutturali nel glomerulo (aumento della matrice extracellulare, ispessimento della membrana basale, espansione mesangiale, fibrosi).
Fase preclinica: microalbuminuria persistente con normale funzione renale.
Fase clinica: macroalbuminuria, ipertensione arteriosa e graduale declino della funzione renale. Inizialmente identificata da Kimmelstiel e Wilson come glomerulosclerosi glomerulare, che in realtà rappresenta solo lo stadio finale della malattia. Recentemente sono state descritte anche forme non proteinuriche di nefropatia diabetica che evolvono anch’esse ad insufficienza renale cronica.
Fase preclinica (stadio I-III)
Stadio I – Nefropatia con iperfiltrazione glomerulare (sempre presente nel diabete di tipo I).
Durata: varaibile
Sintomi: poliuria e glicosuria (nelle fasi di scompenso metabolico), microalbuminuria, iperfiltrazione (eGFR>160ml/min)
Istologia:ipertrofia glomerulare
Patogenesi: ipertensione glomerulare
Fase preclinica (stadio I-III)
Stadio II– Nefropatia silente
Durata: inizia a uno-due anni dall’insorgenza del diabete.
Sintomi: microalbuminuria e iperfiltrazione in occasione di sforzi
fisici ed eccessi alimentari.
Istologia: ispessimento della membrana basale e aumento del mesangio.
Patogenesi:aumentata sintesi della membrana basale e proliferazione mesangiale.
Fase preclinica (stadio I-III)
Stadio III- Nefropatia incipiente
Durata: da 10 a 20 anni
Sintomi: microalbuminuria costante (30/300 mg/24 ore),inizia la riduzione delle eGFR, insorgenza di ipertensione arteriosa, in particolare durante sforzi fisici
Istologia: ipertrofia glomerulare, ispessimento della membrana basale, aumento del mesangio
Patogenesi: iniziale occlusione glomerulare
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Fase clinica ( stadio IV-V)
Stadio IV: nefropatia conclamata
Durata: in genere dopo i 20 anni di malattia
Sintomi: proteinuria con macroalbuminuria
(30-300 mg/24 ore) prgressiva riduzione del eGFR (fino a 10-15 ml/min), ipertensione arteriosa costante di vario grado (prevalentemente sistolica)
Istologia: sclerosi glomerulare progressiva con ipertrofia dei restanti glomeruli, infiltrati interstiziali
Patogenesi: progressiva occlusione glomerulare
Fase clinica (stadio IV-V)
Stadio V: Nefropatia conclamata
Durata: segue la fase IV
Sintomi: proteinuria con macroalbuminuria (30-300 mg/24 ore), evoluzione a insufficienza renale terminale (< 10 ml/min),
ipertensione arteriosa costante di vario grado (prevalentemente sistolica) più sindrome uremica
Istologia: sclerosi glomerulare e fibrosi interstiziale
Patogenesi: occlusione glomerulare totale
Gli interventi efficaci nel rallentare la progressione della microalbuminuria verso la nefropatia manifesta comprendono: normalizzazione della glicemia, stretto controllo pressorio, somministrazione di Ace-inibitori e/o antagonisti dei recettori dell’angiotensina II. Un miglior controllo glicemico riduce la velocità alla quale la microalbuminuria compare e progredisce sia nel DM di tipo I che nel DM di tipo 2. Tuttavia, una volta che la nefropatia è manifesta non è chiaro se un buon controllo glicemico rallenterà la progressione della malattia renale. Durante la fase di declino della funzione renale, la richiesta di insulina può diminuire poiché il rene è un sito di degradazione dell’insulina. Inoltre, i farmaci ipoglicemizzanti (sulfoniluree e metformina) possono accumularsi e sono controindicati nell’insufficienza renale. Lo stretto controllo pressorio riduce l’escrezione di albumina e rallenta il declino della funzione renale. La pressione arteriosa dovrebbe essere mantenuta al di sotto dei 130/85 mmHg nei pazienti diabetici senza proteinuria. Una pressione arteriosa leggermente inferiore (120/80) dovrebbe essere l’obiettivo per i soggetti con microalbuminuria o nefropatia conclamata. Gli Ace-inibitori riducono la progressione della nefropatia conclamata negli individui con DM di tipo 1 di tipo 2 e dovrebbe essere prescritti negli individui con diabete tipo 1 o di tipo 2 e microalbuminuria.
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