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| Year : 2021 | Volume
: 32
| Issue : 2 | Page : 584-585 |
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| Is clinical diagnosis of diabetic kidney disease through persistent albuminuria is superseded by histopathological footprints? |
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Arwa Ahmed Al-Qahtani1, Abdulkarem Awad S. Alenzi1, Akbar Shoukat Ali2
1 Prince Mohammed bin Abdulaziz Hospital, Riyadh, Saudi Arabia
2 Aga Khan University Hospital, Karachi, Pakistan
Click here for correspondence address and email
| Date of Web Publication | 11-Jan-2022 |
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How to cite this article:
Al-Qahtani AA, S. Alenzi AA, Ali AS. Is clinical diagnosis of diabetic kidney disease through persistent albuminuria is superseded by histopathological footprints?. Saudi J Kidney Dis Transpl 2021;32:584-5 |
How to cite this URL:
Al-Qahtani AA, S. Alenzi AA, Ali AS. Is clinical diagnosis of diabetic kidney disease through persistent albuminuria is superseded by histopathological footprints?. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jun 26];32:584-5. Available from: https://www.sjkdt.org/text.asp?2021/32/2/584/335476 |
To the Editor,
Diabetic kidney disease (DKD), also referred to as diabetic nephropathy, is a leading cause of morbidity and mortality globally. DKD is a clinical condition characterized by persistent albuminuria (>300 mg/24 h), progressive deterioration in glomerular filtration rate (GFR), and ultimately end-stage renal disease (ESRD).[1],[2] Nearly 20%–40% of diabetic patients [both type 1 or type 2 diabetes mellitus (DM)] progress to DKD. In fact, diabetes and associated proteinuria not only increase the chances of mortality by the progression of ESRD but also augment the risk of cardiovascular disease which is predominantly frequent in type 2 DM patients.
The advancement of DKD from proteinuria to ESRD is irrevocable. Thus, timely identification of the course of the disease is enormously imperative. And for decades, albuminuria was considered as probably the earliest sign of the onset of DKD.[3] However, lately questions have been raised against the concept of diagnosing DKD solely on the grounds of albuminuria and whether changes in the kidney microstructure correlate with albuminuria has been questioned. Notwithstanding that albuminuria is the earliest clinical sign of DKD and is associated with the development and progression of DKD, albuminuria could not prognosticate the renal ramifications in patients with DM independently.[4] A study by Caramori et al sought to ascertain whether early glome-rular lesions could determine the progression of DKD in normoalbuminuric diabetic patients. They demonstrated that quantitative assessment of kidney histopathology considerably predicts the development and advancement of type 1 DM to clinical DKD in normoalbuminuric patients.[5] Besides other histopathological markers, decrease in podocytes number has also been suggested to precede albuminuria in patients with type 2 DM.[2] Steinke et al revealed no significant differences on renal histology in type 1 DM patients with initial normoalbuminuria followed by microalbuminuria or persistent microalbuminuria or spontaneous return to normoalbuminuria.[6] Conversely, renal lesions in type 2 DM have also been described as heterogeneous.[7] It can be safely deduced from the above evidence that normoalbuminuria does not exclude the presence of renal microstructure lesions, and equally, albuminuria does not essentially foretell the existence of renal microstructural deviations.
Although the sorting of DKD established on albuminuria and estimated GFR (eGFR) level is quite straightforward and offers prediction and facilitates therapeutic decision making, one should be aware that it is inconsistent as well. However, regardless of available evidence that albuminuria may not demonstrate the true picture of DKD as several diabetic patients remain normoalbuminuric after reaching a persistent low GFR <60 mL/min, albuminuria remains the most conventional method of DKD screening.[4] In the not-too-distant past, a histopathological study by Comai et al suggested that renal microstructure damage is evident in diabetic patients in very early stages of CKD (Class I and II) with absent albuminuria and eGFR >60 mL/min/1.73 m2.[2]
In conclusion, the progression of uncomplicated DM to renal insult and ultimately ESRD or death is a longstanding process, and early changes and risk of disease progression is very much evident in renal microstructure and might not be noticeable through classic clinical findings such as albuminuria. Several diabetic patients may remain normoalbuminuric even with a persistent low GFR of <60 mL/min. Therefore, efforts must be directed to investigate the frequency of histological renal microstructure insults and their classification reflecting DKD with clinically non-evident nephropathy. This strategy will certainly shape the roadmap for nephrologists to expedite the early detection of DKD and improve the risk stratification and facilitate therapeutic decision making accordingly.
Conflict of interest: None declared.
 References | |  |
| 1. | Persson F, Rossing P. Diagnosis of diabetic kidney disease: state of the art and future perspective. Kidney Int Suppl (2011) 2018;8:2-7.  |
| 2. | Comai G, Malvi D, Angeletti A, et al. Histological evidence of diabetic kidney disease precede clinical diagnosis. Am J Nephrol 2019; 50:29-36. |
| 3. | Aldukhayel A. Prevalence of diabetic nephropathy among type 2 diabetic patients in some of the Arab countries. Int J Health Sci (Qassim) 2017;11:1-4. |
| 4. | MacIsaac RJ, Ekinci EI, Jerums G. Progressive diabetic nephropathy. How useful is micro- albuminuria? Contra. Kidney Int 2014;86:50-7. |
| 5. | Caramori ML, Parks A, Mauer M. Renal lesions predict progression of diabetic nephropathy in type 1 diabetes. J Am Soc Nephrol 2013;24: 1175-81. |
| 6. | Steinke JM, Sinaiko AR, Kramer MS, et al. The early natural history of nephropathy in type 1 diabetes: III. Predictors of 5-year urinary albumin excretion rate patterns in initially normoalbuminuric patients. Diabetes 2005;54: 2164-71. |
| 7. | Fioretto P, Mauer M, Brocco E, et al. Patterns of renal injury in NIDDM patients with microalbuminuria. Diabetologia 1996;39:1569- 76. |
Correspondence Address:
Akbar Shoukat Ali
Aga Khan University Hospital, Karachi
Pakistan
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1319-2442.335476
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