<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">OJNeph</journal-id><journal-title-group><journal-title>Open Journal of Nephrology</journal-title></journal-title-group><issn pub-type="epub">2164-2842</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/ojneph.2023.134032</article-id><article-id pub-id-type="publisher-id">OJNeph-128927</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  Contribution to the Study of Diabetic Kidney Disease in a Sub-Saharan Environment: An Example of the Aristide Le Dantec University Hospital in Dakar
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Ahmed</surname><given-names>Tall Lemrabott</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Maria</surname><given-names>Faye</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Niakhaleen</surname><given-names>Keita</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Seynabou</surname><given-names>Diagne</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Moustapha</surname><given-names>Faye</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Bacary</surname><given-names>Ba</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Abdou</surname><given-names>Niang</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>El</surname><given-names>Hadji Fary Ka</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib></contrib-group><aff id="aff2"><addr-line>Nephrology Department, Dalal Jamm National Hospital Center, Dakar, Senegal</addr-line></aff><aff id="aff1"><addr-line>Nephrology Department, Aristide Le Dantec University Hospital, Dakar, Senegal</addr-line></aff><pub-date pub-type="epub"><day>20</day><month>10</month><year>2023</year></pub-date><volume>13</volume><issue>04</issue><fpage>339</fpage><lpage>348</lpage><history><date date-type="received"><day>2,</day>	<month>September</month>	<year>2023</year></date><date date-type="rev-recd"><day>5,</day>	<month>November</month>	<year>2023</year>	</date><date date-type="accepted"><day>8,</day>	<month>November</month>	<year>2023</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  Introduction: Diabetic kidney disease (DKD) is a leading cause of chronic kidney disease and dialysis admission. Few studies are available in Sub-Saharan Africa. The objective of this work was to study the epidemiological, clinical, diagnostic and therapeutic characteristics of DKD in our context. 
  Patients and Methods: We conducted an observational, exhaustive and retrospective study focusing on diabetic patients seen in consultation or hospitalized in the Nephrology Department of at the Aristide Le Dantec University Hospital in Dakar during a period of 5 years from January 1, 2017 to December 31, 2021. 
  Results: Of 4735 patients seen during the study period, 491 had DKD, 
  i.e. a hospital prevalence of 10.36%. The average age was 59.1 &#177; 11.4 years with a sex ratio of 0.95. Type 2 diabetes predominated with 93.4%. The average duration of diabetes was 11.5 &#177; 7.6 years. Diabetes was associated with high blood pressure in 78.81% of cases, dyslipidemia in 23.2% of cases, active smoking in 6.7% of cases and obesity in 1.6% of cases. Renal failure was the main reason for referral 72.3%. One hundred and forty-eight patients (30.1%) had uncontrolled diabetes. Macroalbuminuria was found in 64.8% and microalbuminuria in 18.7% of cases. One hundred and eighty-five patients (37.7%) were in Stage V of kidney disease and 137 patients were in Stage III (18.1% in Stage IIIb and 9.8% in Stage IIIa). Diabetic nephropathy was the main etiology at 61.30%. Nephropathy was mixed (diabetic and hypertensive) in 18.12 cases. Renin-angiotensin-aldosterone system (RAAS) blockers were prescribed in 83.5% of patients. 
  Conclusion: The different etiologies encountered during the study show the diversity of diabetic kidney disease. Diabetic nephropathy is not the only kidney damage that can occur in diabetics in our context.
 
</p></abstract><kwd-group><kwd>Diabetic Kidney Disease (DKD)</kwd><kwd> Microalbuminuria</kwd><kwd> Diabetic Nephropathy</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>Diabetic kidney disease (DKD) is the set of kidney lesions observed in diabetics [<xref ref-type="bibr" rid="scirp.128927-ref1">1</xref>] . These lesions can occur in all structures of the nephron: glomeruli, renal vessels, tubules and renal interstitium.</p><p>The risk factors for DKD are not very specific. Alongside essential chronic hyperglycemia, we find other vascular risk factors (tobacco, hypertension, dyslipidemia). It is necessary to add a family history of diabetes with nephropathy and factors, such as markers of inflammation, oxidative stress, advanced glycosylation products, hyperuricemia, cardiovascular abnormalities, and urinary tubular markers [<xref ref-type="bibr" rid="scirp.128927-ref2">2</xref>] .</p><p>DKD remains a major public health issue; it represents 22% of the causes of Stage V chronic kidney disease, and its share has increased over the last decade [<xref ref-type="bibr" rid="scirp.128927-ref3">3</xref>] . The occurrence of kidney damage in diabetics is associated with an increased risk of cardiovascular morbidity and mortality, starting at the microalbuminuria stage [<xref ref-type="bibr" rid="scirp.128927-ref4">4</xref>] .</p><p>The progression of diabetes in Senegal is much like elsewhere in the world. The first nationwide survey conducted in 2015 showed a prevalence of 3.4% in people aged 18 - 69 years and 7.9% in those over 45 years. The majority had type 2 diabetes [<xref ref-type="bibr" rid="scirp.128927-ref5">5</xref>] . These patients are often referred to nephrology at advanced stages of CKD (Stages 4 and 5) as evidenced by a previous study in our division of nephrology [<xref ref-type="bibr" rid="scirp.128927-ref6">6</xref>] .</p><p>In Senegal, as in most countries in Sub-Saharan Africa, there have been publications on diabetic nephropathy. However, to our knowledge, DKD has not yet been studied in our country. This is why we set ourselves the objectives here of determining its prevalence and describing its clinical and paraclinical aspects.</p></sec><sec id="s2"><title>2. Patients and Methods</title><p>This was an observational, exhaustive and retrospective study, based on patient files, over a period of 5 years, from January 1, 2017 to December 31, 2021. The study population consisted of diabetic patients received in consultation or hospitalized in the Nephrology Department at the Aristide Le Dantec University Hospital in Dakar during the study period.</p><p>We included diabetic patients with kidney disease referred or admitted to the Nephrology Department during the study period. Unusable files were excluded.</p><p>Data was collected on a pre-established and standardized survey form for all medical records. From this sheet, we collected epidemiological, clinical, biological, and morphological data.</p><p>MRD was defined as any chronic renal damage (&gt;3 months) occurring in a diabetic patient.</p><p>The data collected was entered using the Sphinx software serving as a database and the SPSS (Statistical Package for Social Sciences) software. The variables are compared using the KHI 2 or Fischer test depending on their applicability condition. The difference was statistically significant at a p &lt; 0.05.</p><p>Local ethics committee gave its approval for the study.</p></sec><sec id="s3"><title>3. Results</title><p>During the study period, 4735 patients were consulted, among whom 491 had diabetic kidney disease, representing a hospital prevalence of 10.36%. The average age was 59.1 &#177; 11.4 years with extremes of 25 and 90 years. The age group of 61 to 70 years was the most representative (<xref ref-type="fig" rid="fig1">Figure 1</xref>). The sex ratio was 0.95 with 51.3% female patients and 48.7% male. Type 2 diabetes was found in 459 patients (93.4%), type 1 diabetes in 32 patients (6.6%). The average duration of diabetes was 11.5 &#177; 7.6 years. Hypertension was present in 78.81% of patients. Other comorbidities and chronic complications of diabetes are shown in <xref ref-type="table" rid="table1">Table 1</xref>.</p><p>Renal insufficiency represented 72.3% of the reasons for consultation followed by renal oedematous syndrome (12.8%).</p><p>The main syndromes found at the clinic were: chronic glomerular nephropathy syndrome in 81.6%, uremia in 27.7%, and anemic syndrome (35.8%). Mean systolic blood pressure was 173.2 &#177; 21.1 mmHg with extremes of 130 - 270 mmHg. Mean diastolic blood pressure was 94.6 &#177; 13.9 mmHg with extremes of 57 - 140 mmHg.</p><table-wrap id="table1" ><label><xref ref-type="table" rid="table1">Table 1</xref></label><caption><title> Epidemiological parameters, comorbidities, and diabetic complications of the study population</title></caption><table><tbody><thead><tr><th align="center" valign="middle" >Parameters</th><th align="center" valign="middle" >Results</th></tr></thead><tr><td align="center" valign="middle" >Epidemiological parameters</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Mean age</td><td align="center" valign="middle" >59.1 &#177; 11.4 years</td></tr><tr><td align="center" valign="middle" >Sex-ratio (male/female)</td><td align="center" valign="middle" >0.95 (51.3%/48.7%)</td></tr><tr><td align="center" valign="middle" >Type 1 diabetes</td><td align="center" valign="middle" >6.6%</td></tr><tr><td align="center" valign="middle" >Type 2 diabetes</td><td align="center" valign="middle" >93.4%</td></tr><tr><td align="center" valign="middle" >Average duration of diabetes</td><td align="center" valign="middle" >11.5 &#177; 7.6 years</td></tr><tr><td align="center" valign="middle" >Comorbidities</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Hypertension</td><td align="center" valign="middle" >78.81%</td></tr><tr><td align="center" valign="middle" >Smoking</td><td align="center" valign="middle" >6.7%</td></tr><tr><td align="center" valign="middle" >Obesity</td><td align="center" valign="middle" >1.6%</td></tr><tr><td align="center" valign="middle" >Dyslipidemia</td><td align="center" valign="middle" >23.2%</td></tr><tr><td align="center" valign="middle" >Stroke</td><td align="center" valign="middle" >7.1%</td></tr><tr><td align="center" valign="middle" >Heart failure</td><td align="center" valign="middle" >19.6%</td></tr><tr><td align="center" valign="middle" >Gout</td><td align="center" valign="middle" >1.22%</td></tr><tr><td align="center" valign="middle" >Cancer</td><td align="center" valign="middle" >1.62%</td></tr><tr><td align="center" valign="middle" >Sickle cell disease</td><td align="center" valign="middle" >1.01%</td></tr><tr><td align="center" valign="middle" >Chronic complications of diabetes</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >&#183; Diabetic microangiopathies</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Diabetic retinopathy</td><td align="center" valign="middle" >59.87%</td></tr><tr><td align="center" valign="middle" >Diabetic neuropathy</td><td align="center" valign="middle" >7.94%</td></tr><tr><td align="center" valign="middle" >&#183; Diabetic microangiopathies</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Peripheral arterial disease (PAD)</td><td align="center" valign="middle" >14.86%</td></tr><tr><td align="center" valign="middle" >Coronary heart disease</td><td align="center" valign="middle" >6.31%</td></tr><tr><td align="center" valign="middle" >Diabetes therapy on admission</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle" >Insulin</td><td align="center" valign="middle" >40.32%</td></tr><tr><td align="center" valign="middle" >Oral antidiabetic drugs</td><td align="center" valign="middle" >32.99%</td></tr><tr><td align="center" valign="middle" >Diabetic diet alone</td><td align="center" valign="middle" >26.68%</td></tr></tbody></table></table-wrap><p>Biologically, the average blood sugar level was 1.5 &#177; 0.8 g/l with extremes of 0.5 to 7.3 g/l with an average glycated hemoglobin of 8.0% &#177; 2.7%. The mean serum creatinine was 49.3 &#177; 52.7 mg/l with a mean GFR (according to CKD-EPI) of 28.7 &#177; 25.5 ml/min. Stage V of CKD was the most representative (<xref ref-type="fig" rid="fig2">Figure 2</xref>). Mean proteinuria was 2.1 &#177; 2.4 g/24h with ranges from 0.15 to 12.0 g/24h. Mean Calcemia and Phosphataemia were 87.2 &#177; 11.6 mg/l and 46.9 &#177; 23 mg/l respectively. The other biological parameters are shown in <xref ref-type="table" rid="table2">Table 2</xref>.</p><table-wrap id="table2" ><label><xref ref-type="table" rid="table2">Table 2</xref></label><caption><title> Biological characteristics of the study population</title></caption><table><tbody><thead><tr><th align="center" valign="middle"  rowspan="2"  >Parameters</th><th align="center" valign="middle" >Results</th></tr></thead><tr><td align="center" valign="middle" >Mean, SD or percentage, extremes</td></tr><tr><td align="center" valign="middle" >Blood glucose</td><td align="center" valign="middle" >1.5 &#177; 0.8 (0.5 - 7.3)</td></tr><tr><td align="center" valign="middle" >Glycated hemoglobin</td><td align="center" valign="middle" >8.0 &#177; 2.7 (3.5 - 14)</td></tr><tr><td align="center" valign="middle" >Blood urea nitrogen</td><td align="center" valign="middle" >1.2 &#177; 0.9 (0.15 - 8.64)</td></tr><tr><td align="center" valign="middle" >Serum creatinine</td><td align="center" valign="middle" >49.3 &#177; 52.7 (3.3 - 387)</td></tr><tr><td align="center" valign="middle" >eGFR</td><td align="center" valign="middle" >28.7 &#177; 25.5 (1 - 133)</td></tr><tr><td align="center" valign="middle" >Calcemia</td><td align="center" valign="middle" >87.2 &#177; 11.6 (30 - 109)</td></tr><tr><td align="center" valign="middle" >Phosphataemia</td><td align="center" valign="middle" >46.9 &#177; 23 (15.4 - 22.5)</td></tr><tr><td align="center" valign="middle" >Hemoglobin</td><td align="center" valign="middle" >9.7 &#177; 2.5 (3.6 - 16.4)</td></tr><tr><td align="center" valign="middle" >Total cholesterol</td><td align="center" valign="middle" >2.1 &#177; 0.7 (0.8 - 4.6)</td></tr><tr><td align="center" valign="middle" >LDL cholesterol</td><td align="center" valign="middle" >1.4 &#177; 0.6 (0.4 - 3.8)</td></tr><tr><td align="center" valign="middle" >HDL cholesterol</td><td align="center" valign="middle" >0.5 &#177; 0.2 (0.1 - 4.2)</td></tr><tr><td align="center" valign="middle" >Triglyceride</td><td align="center" valign="middle" >1.1 &#177; 0.6 (0.1 - 4.2)</td></tr><tr><td align="center" valign="middle" >Natremia</td><td align="center" valign="middle" >136.2 &#177; 6.6 (101 - 156)</td></tr><tr><td align="center" valign="middle" >Kalemia</td><td align="center" valign="middle" >4.7 &#177; 0.9 (1.8 - 7.8)</td></tr><tr><td align="center" valign="middle" >Chloremia</td><td align="center" valign="middle" >103.4 &#177; 7.6 (62 - 139)</td></tr><tr><td align="center" valign="middle" >Microalbuminuria</td><td align="center" valign="middle" >285.5 &#177; 732.4 (30 - 300)</td></tr><tr><td align="center" valign="middle" >Macroalbuminuria</td><td align="center" valign="middle" >2.1 &#177; 2.4 (0.3 - 12 g/24h)</td></tr><tr><td align="center" valign="middle" >Hematuria</td><td align="center" valign="middle" >5.1%</td></tr><tr><td align="center" valign="middle" >Leukocyturia</td><td align="center" valign="middle" >6.3%</td></tr><tr><td align="center" valign="middle" >Urinary infection</td><td align="center" valign="middle" >9.8%</td></tr></tbody></table></table-wrap><p>Of all the DKDs, diabetic nephropathy was found in 301 patients (61.30%) followed by the mixed nephropathy in 89 patients (18.12%). The other attacks are represented in <xref ref-type="table" rid="table3">Table 3</xref>.</p><p>Therapeutically, renin-angiotensin-aldosterone system (RAAS) blockers were prescribed in 83.5% of patients. Insulin therapy was prescribed in 39.9% of cases. Concerning oral antidiabetics: metformin was prescribed in 23.8% of cases, sulphonylureas in 7.3% of cases, and DPP-4 inhibitors in 1.0% of cases.</p><p>At the reporting date, mortality was 4.3%. Admission to dialysis was noted in 13.2% of patients. The others are still followed in nephrology consultation.</p><p>Analytically, the presumptive diagnosis of diabetic nephropathy was statistically associated with the absence of haematuria (p &lt; 0.001) and leukocyturia (p &lt; 0.001) and the presence of nephrotic syndrome (p &lt; 0.003) (<xref ref-type="table" rid="table4">Table 4</xref>).</p><table-wrap id="table3" ><label><xref ref-type="table" rid="table3">Table 3</xref></label><caption><title> Distribution of patients according to etiology found</title></caption><table><tbody><thead><tr><th align="center" valign="middle"  colspan="2"  >Renal damage</th><th align="center" valign="middle" >Number</th><th align="center" valign="middle" >Percentage (%)</th></tr></thead><tr><td align="center" valign="middle"  colspan="2"  >Diabetic nephropathy</td><td align="center" valign="middle" >301</td><td align="center" valign="middle" >61.30</td></tr><tr><td align="center" valign="middle"  colspan="2"  >Mixed nephropathy</td><td align="center" valign="middle" >89</td><td align="center" valign="middle" >18.12</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Atherosclerotic renal artery</td><td align="center" valign="middle" >Hypertensive nephropathy</td><td align="center" valign="middle" >61</td><td align="center" valign="middle" >12.42</td></tr><tr><td align="center" valign="middle" >Renal artery stenosis</td><td align="center" valign="middle" >3</td><td align="center" valign="middle" >0.62</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Tubulointerstitial nephritis</td><td align="center" valign="middle" >Pyelonephritis</td><td align="center" valign="middle" >31</td><td align="center" valign="middle" >6.31</td></tr><tr><td align="center" valign="middle" >Drug toxicity</td><td align="center" valign="middle" >6</td><td align="center" valign="middle" >1.22</td></tr><tr><td align="center" valign="middle"  colspan="2"  >Total</td><td align="center" valign="middle" >491</td><td align="center" valign="middle" >100.0</td></tr></tbody></table></table-wrap><table-wrap id="table4" ><label><xref ref-type="table" rid="table4">Table 4</xref></label><caption><title> Association between clinico-biological variables and the diagnosis of diabetic nephropathy</title></caption><table><tbody><thead><tr><th align="center" valign="middle" ></th><th align="center" valign="middle" ></th><th align="center" valign="middle" >OR (95% CI)</th><th align="center" valign="middle" >p</th></tr></thead><tr><td align="center" valign="middle" >Age (years)</td><td align="center" valign="middle" ></td><td align="center" valign="middle" >0.99 (0.97 - 1.01)</td><td align="center" valign="middle" >0.212</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Sex</td><td align="center" valign="middle" >Women</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >0.685</td></tr><tr><td align="center" valign="middle" >Men</td><td align="center" valign="middle" >1.08 (0.75 - 1.54)</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Type of diabetes</td><td align="center" valign="middle" >Type 1</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >0.930</td></tr><tr><td align="center" valign="middle" >Type 2</td><td align="center" valign="middle" >1.61 (0.28 - 4.00)</td></tr><tr><td align="center" valign="middle" >Duration of diabetes</td><td align="center" valign="middle" ></td><td align="center" valign="middle" >1.01 (0.98 - 1.03)</td><td align="center" valign="middle" >0.646</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Metabolic complications</td><td align="center" valign="middle" >No</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle" >0.063</td></tr><tr><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" >1.52 (0.98 - 2.36)</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Diabetic retinopathy</td><td align="center" valign="middle" >No</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  ></td></tr><tr><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" ></td></tr><tr><td align="center" valign="middle"  rowspan="2"  >High blood pressure</td><td align="center" valign="middle" >No</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >0.735</td></tr><tr><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" >0.93 (0.6 - 1.43)</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Hematuria</td><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >&lt; 0.001</td></tr><tr><td align="center" valign="middle" >No</td><td align="center" valign="middle" >1.98 (1.34 - 2.94)</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Leukocyturia</td><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >&lt; 0.001</td></tr><tr><td align="center" valign="middle" >No</td><td align="center" valign="middle" >1.98 (1.33 - 2.94)</td></tr><tr><td align="center" valign="middle"  rowspan="2"  >Nephrotic syndrome</td><td align="center" valign="middle" >No</td><td align="center" valign="middle" >Reference</td><td align="center" valign="middle"  rowspan="2"  >0.003</td></tr><tr><td align="center" valign="middle" >Yes</td><td align="center" valign="middle" >2.37 (1.3 - 4.32)</td></tr></tbody></table></table-wrap></sec><sec id="s4"><title>4. Discussion</title><p>The prevalence of DKD followed the global epidemic of obesity and type 2 diabetes mellitus. No region seems to be spared from this scourge, including the Mediterranean region that was until now [<xref ref-type="bibr" rid="scirp.128927-ref7">7</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref8">8</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref9">9</xref>] . DKD is by far the leading cause of end-stage chronic renal failure leading to dialysis treatment. It represents almost 60% in the United States, almost 50% in Asia and almost 40% in Europe [<xref ref-type="bibr" rid="scirp.128927-ref10">10</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref11">11</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref12">12</xref>] . In our context, the prevalence is high (10.36%) but comes second after hypertension that remains the leading cause of CKD in Senegal [<xref ref-type="bibr" rid="scirp.128927-ref13">13</xref>] .</p><p>In our series, the average duration of progression of diabetes was 11.5 &#177; 7.6 years reflecting the natural history of progression of diabetic nephropathy described in the literature. In our series, hypertension was noted in 78.81% of patients. These results are justified by the association of diabetes and hypertension, which both contribute to DKD [<xref ref-type="bibr" rid="scirp.128927-ref1">1</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref14">14</xref>] .</p><p>In our context, the main reasons for consultations were impaired renal function followed by macroalbuminuria. This demonstrates a late referral of diabetic patients to nephrology consultations in Sub-Saharan Africa, as evidenced by the study of Adebamowo et al. [<xref ref-type="bibr" rid="scirp.128927-ref15">15</xref>] . Hence, there is a need to establish multidisciplinary management strategies for diabetic patients in Sub-Saharan Africa to better prevent DKD.</p><p>The diagnosis was mainly made at Stage V (37.7% of patients) then at Stage III 27.9% and at Stage IV 22.0%. This result demonstrates the delay in diagnosing patients in our hospitals.</p><p>In our series, diabetic nephropathy represented the first attack (58.9%) followed by mixed nephropathy (diabetic and hypertensive) in 13.0% of cases. A third of type 2 diabetic patients with macroproteinuria have histological lesions that are not solely related to diabetic nephropathy [<xref ref-type="bibr" rid="scirp.128927-ref16">16</xref>] . Associated histological lesions are also possible, notably diabetic nephropathy and hypertensive nephropathy (nephroangiosclerosis) can coexist [<xref ref-type="bibr" rid="scirp.128927-ref16">16</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref17">17</xref>] [<xref ref-type="bibr" rid="scirp.128927-ref18">18</xref>] . Only renal biopsy therefore makes it possible to correctly classify the histological involvement but the proportion of diabetics benefiting from a renal biopsy is low (&lt;20%) while the clinical diagnosis of nephropathy varies depending on the type of diabetes.</p><p>Renin-Angiotensin-Aldosterone System Blockers were prescribed in 83.5% of patients in our cohort. We need to sensitise more our general practitioners aware of the usefulness of prescribing these molecules, especially at the onset of microalbuminuria and/or an association with hypertension.</p><p>Sodium-glucose cotransporter-2 (SGLT2) inhibitors or gliflozins occupy an increasingly important place in the treatment of patients with type 2 diabetes. This is particularly the case in patients with proven cardiovascular disease, heart failure, chronic kidney disease, or in patients with a combination of risk factors exposing them to such complications [<xref ref-type="bibr" rid="scirp.128927-ref19">19</xref>] .</p><p>SGLT2 inhibitors provided evidence of nephroprotection, demonstrated by a reduction in albuminuria, a lesser decline in long-term renal function and a reduction in progression to ESRD or death from renal causes. This nephrological benefit adds to the CV protection already described, including a reduction in the incidence of major CV events and, above all, hospitalizations for heart failure. The favourable renal effects are consistent in the different subgroups studied, separated by the presence or absence of heart failure at inclusion, by the level of GFR, and by the rate of albuminuria. These remarkably consistent results have given SGLT2 inhibitors pride of place in the latest international recommendations in diabetes, cardiology, and nephrology [<xref ref-type="bibr" rid="scirp.128927-ref20">20</xref>] . As we complete this article, SGLT2 inhibitors are not currently available in Senegal.</p></sec><sec id="s5"><title>5. Conclusion</title><p>In our context, DKD is a public health problem. It remains the 2nd cause of CKD after hypertension. It is dominated by diabetic nephropathy followed by mixed nephropathy (diabetic and hypertensive). Early detection and, above all, multidisciplinary collaboration between nephrologists, diabetologists and general practitioners will reduce its high prevalence in our country.</p></sec><sec id="s6"><title>Conflicts of Interest</title><p>The authors declare no conflicts of interest regarding the publication of this paper.</p></sec><sec id="s7"><title>Cite this paper</title><p>Lemrabott, A.T., Faye, M., Keita, N., Diagne, S., Faye, M., Ba, B., Niang, A. and Ka, E.H.F. (2023) Contribution to the Study of Diabetic Kidney Disease in a Sub-Saharan Environment: An Example of the Aristide Le Dantec University Hospital in Dakar. Open Journal of Nephrology, 13, 339-348. https://doi.org/10.4236/ojneph.2023.134032</p></sec></body><back><ref-list><title>References</title><ref id="scirp.128927-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Chen, Y., Lee, K., Ni, Z. and He, J.C. (2020) Diabetic Kidney Disease: Challenges, Advances, and Opportunities. 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