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| Year : 2021 | Volume
: 32
| Issue : 2 | Page : 590-591 |
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| The cheloid scars, a cause of high renin hypertension in black subjects? |
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Richard Loumingou1, Ida Aurélie Lenga Loumingou2
1 Department Nephrology, Brazzaville University Hospital Center, Brazzaville, Congo
2 Department Dermatology, Brazzaville University Hospital Center, Brazzaville, Congo
Click here for correspondence address and email
| Date of Web Publication | 11-Jan-2022 |
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How to cite this article:
Loumingou R, Lenga Loumingou IA. The cheloid scars, a cause of high renin hypertension in black subjects?. Saudi J Kidney Dis Transpl 2021;32:590-1 |
How to cite this URL:
Loumingou R, Lenga Loumingou IA. The cheloid scars, a cause of high renin hypertension in black subjects?. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jan 25];32:590-1. Available from: https://www.sjkdt.org/text.asp?2021/32/2/590/335479 |
To the Editors,
Keloid scars are a pathology of the black subject. They result from an alteration in the normal healing process and are formed as a result of a loss of substance or an inflammatory process in the skin.[1] Studies of keloids have led to advances in the understanding of racial differences in high blood pressure. The same growth factors involved in keloid pathogenesis are involved in nephrosclerosis and atherogenesis. A higher prevalence of renal impairment and high blood pressure has been associated with black subjects with keloids.[2] Hypertension (HTN) in black subjects differs from that in white subjects in terms of severity, early complications, and high prevalence, and is also known to be salt-dependent and low-renin.[3] The objective of this work was to report biological and therapeutic elements that would make it possible to evoke the high renin character of HTN of black subjects carrying keloids to optimize the physiopathological understanding and the global management of this pathology of black subjects.
We conducted a cross-sectional, analytical study from January 2012 to December 2016 at the Brazzaville University Hospital Center. We included hypertensive patients with keloids, and hypertensive patients treated with angiotensin converting enzyme inhibitors (ACE inhibitors) or angiotensin II antagonists [angiotensin receptor blockers (ARBs)] as monotherapy. Patients on corticosteroids, diuretics, calcium channel blockers, normotensive patients, patients with renal insufficiency, and patients with renal cysts were excluded from the study.
Parameters studied were; creatinine, MDRD creatinine clearance, blood ionogram, urine ionogram, renal ultrasound. Fifty-eight patients with keloid scars were examined during the study period 15 patients met our criteria the sex ratio male-female was 1.9, 13 patients were biologically balanced on ACE inhibitor monotherapy or ARAII [Table 1]. Twelve out of 15 patients had low kalemia, three out of 15 patients had normal kalemia, kaliuresis was elevated in 13 out of 15 patients. Natriuresis was low in 10 out of 15 patients, normal in four patients, and high in one patient.
The low renin character of the black subject’s HTN is affirmed by the ineffectiveness of the molecules that slow down the reninangiotensin-aldosterone system in lowering blood pressure. There are several arguments to suggest the high renin character of HTN in black subjects with keloids. Keloids are linked to a healing defect due to excessive collagen production. The work of Ogawa and Akaishi[4] has suggested a relevant link between endo-thelial dysfunction and the pathogenesis of keloid scars. Increases in circulating and urinary angiotensin levels have also been demonstrated in patients with keloids. In our observations, the high renin hypothesis of HTN in patients with keloids is based on the efficacy of ACE inhibitors or ARBs prescribed as monotherapy; the tendency to hypokalemia found in patients associated with urinary potassium leakage and decreased urinary sodium excretion was consistent with hyperreninism. HLAB35 is associated with black subjects responding with ACE inhibitors.[5]
Our study is preliminary. Larger studies with more exhaustive investigations are necessary to affirm the high renin character of HTN of black subjects carrying keloids. Several hypotheses could be evoked. Relation between keloids scars and HLAB35? Renin stimulation by chronic vascular inflammatory processes related to the genesis of keloid scars? Confirmation of these hypotheses will affirm the role of ACE inhibitors and ARBs as a first-line therapeutic class in hypertensive black subjects with keloids.
Conflict of interest: None declared.
 References | |  |
| 1. | Berman B, Maderal A, Raphael B. Keloids and hypertrophic scars: Pathophysiology, classification, and treatment. Dermatol Surg 2017;43 Suppl 1:S3-18.  |
| 2. | Dustan HP. Does keloid pathogenesis hold the key to understanding black/white differences in hypertension severity? Hypertension 1995;26: 858-62. |
| 3. | Amah G, Levy BI. Particularités de l’hypertension artérielle du sujet noir Africain. Sang Thromb Vaiss 2007;19. |
| 4. | Ogawa R, Akaishi S. Endothelial dysfunction may play a key role in keloid and hypertrophic scar pathogenesis – Keloids and hypertrophic scars may be vascular disorders. Med Hypotheses 2016;96:51-60. |
| 5. | Gerbase-DeLima M, Paiva RL, Bortolotto LA, Bernardes-Silva H, De Lima JJ. Human leukocyte antigens and malignant essential hypertension. Am J Hypertens 1998;11:729-31. |
Correspondence Address:
Richard Loumingou
Departments Nephrology, Brazzaville University Hospital Center, Brazzaville
Congo
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DOI: 10.4103/1319-2442.335479 PMID: 35017361 
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