Rapid decline of renal function in patients with type 2 diabetes with heavy proteinuria: a report of three cases

Abstract

BackgroundAlthough there is a large volume of literature regarding the definition and epidemiology of.Type 2 diabetes nephropathy (T2DN). There has been a paucity of data focused on the rate of transition of T2 DN. Based on our personal observation a certain percentage of our incident end stage renal disease (ESRD) patients from T2DN experienced a rapid decline of renal function. Their rapid decline nature of glomerular filtration rate (GFR) of 46 to 60 mL/min per 1.73m2 per year have far exceeded the KDIGO definitions of acute kidney injury (abrupt decrease in kidney function occurring over 7 days or less), acute kidney disease (acute or subacute damage and/or loss of kidney function for a duration of between 7 and 90 days after exposure to an acute kidney injury initiating event (Chawla et al Nat Rev Nephrol 241–57 2017) or even rapid decliner (eGFR declines > 5 mL/min per 1.73m2 per year) (Chawla et al Nat Rev Nephrol 241–57 2017; Andrassy Kidney Int 622–623 2013).Case presentationWe describe here three cases of type 2 diabetic patients that have rapid renal deterioration with rate of decline 46 - 60 mL/min per 1.73m2 per year. All the patients are heavily nephrotic. All of the renal biopsies done showed the classical diabetic changes, hypertensive changes, diffuse tubulointerstitial damage, and interstitial nephritis. All of the patients admitted to taking various form of traditional medications in hope of curing their renal disease.ConclusionWe wish to highlight that type 2 diabetics with massive nephrotic range proteinuria have enhanced risk of rapid renal function deterioration. The patients should be educated about the risks of rapid renal function deterioration when there is presence of heavy proteinuria. High grade proteinuria is likely to inflict the diffuse tubulointerstitial inflammation. The interstitial nephritis could be further worsened by traditional supplements consumption. Timely health education and advice must be undertaken to retard this unwanted rapid renal disease progression.

Renal expression of cytokines and chemokines in diabetic nephropathy

“…The slow and continuous decline of renal function is associated with progressive tubulointerstitial damage and renal fibrosis, which is characterized by accumulation of leukocytes, fibroblasts, EMC and tubular atrophy [2,46]. Accumulation of macrophages and lymphocytes in interstitium is critical for tubular and interstitial damage, since these cells are the main sources of proinflammatory and pro-fibrotic cytokines [47,48].…”

“…Diabetic nephropathy (DN) is a chronic microvascular complication that affects about 20 to 30% of patients with type 2 diabetes mellitus (T2DM). It is considered the leading cause of end-stage renal failure requiring renal replacement therapy [1,2], although its pathogenesis has not yet been fully elucidated. Immune and inflammatory mechanisms play important role in the development and progression of DN, which is considered a chronic inflammatory disease [3,4].…”

Clinicopathological features of fast eGFR decliners among patients with diabetic nephropathy

“…[1][2][3] There are two characteristic groups: "rapid decliners" and "no or slow decliners". [4][5][6] In addition, some patients recover kidney function. 4 Fast decliners exhibit fast reduction in kidney function and reach end-stage renal disease (ESRD) in a short period of time, whereas slow decliners preserve a degree of kidney function for an extended period of…”

Accelerated Kidney Aging in Diabetes Mellitus

“…Due to chronic hyperglycemia, hypertension, and proteinuria, 34.8% of patients have a progressive disease with an annual GFR decline of 3:57 ± 1:45 mL/min/1:73 m 2 /year due to chronic hyperglycemia, hypertension, and proteinuria [140]. Significantly, DN patients with heavy proteinuria experience a rapid renal deterioration with the rate of decline of 46-60 mL/min/1.73 m 2 /year [141]. Those represent a more accelerated decline compared to normal biological aging at an average rate of 1 mL per year after 30 years old [142].…”