The hyperfiltration injury that occurs is because the excess glucose filtration is intially reabsorbed and carries Na and Cl alongside it - this results in less Cl delivery to the macula densa and release of renin/dopamine to increase that nephrons filtration - this is in excess of whats needed however, the MD is overreacting and the excess filtration leads to hyperfiltration injury
Tend to get both afferent and efferent arterial hyalinosis - in contrast to HTN which tends to be only afferent (as the cap bed protects the efferent from increased transmitted pressures)