1. bookVolume 1 (2021): Issue 3 (December 2021)
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Journal
eISSN
2719-3500
First Published
30 Jun 2021
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English
access type Open Access

Diabetic nephropathy with crescent: A case report

Published Online: 26 Apr 2022
Volume & Issue: Volume 1 (2021) - Issue 3 (December 2021)
Page range: 125 - 128
Received: 07 Oct 2020
Accepted: 17 Feb 2022
Journal Details
License
Format
Journal
eISSN
2719-3500
First Published
30 Jun 2021
Publication timeframe
4 times per year
Languages
English
Abstract

Diabetic nephropathy is one of the main complications of diabetes, and is also one of the important causes of end-stage renal disease. It is characterized by pathological changes such as thickening of the glomerular basement membrane, expansion of the mesangial matrix, glomerular sclerosis, and hyalinosis of small arteries. However, diabetic nephropathy is rarely accompanied by the formation of a large number of crescents. At this time, renal puncture is required to search for the cause in diabetic nephropathy with worsening renal function. We report a case of diabetic nephropathy with the formation of a large number of crescents.

Keywords

Introduction

Diabetic nephropathy is one of the main complications of diabetes, and is also one of the important causes of end-stage renal disease [1, 2]. It is characterized by functional changes such as glomerular hyperfiltration and proteinuria and structural changes such as thickening of the glomerular basement membrane, mesangial matrix expansion, glomerulosclerosis, and arteriolar hyalinosis [3, 4]. However, diabetic nephropathy is rarely accompanied by the formation of a large number of crescents. We report a case of diabetic nephropathy with the formation of a large number of crescents.

Case Report
First hospitalization (October 25, 2019)

A 50-year-old man was evaluated at the nephrology clinic of the First Affiliated Hospital of Zhengzhou University because of edema of lower extremities.

Two months ago, the patient developed mild edema of both lower limbs without obvious cause, accompanied by increased foam in the urine. He had no symptoms of heart failure, no urinary tract irritation, and no fatigue or gastrointestinal symptoms. The temperature was 36.2°C, the heart rate 78 beats per minute, the blood pressure 146/90 mmHg, height 176 cm, weight 99 kg, and the oxygen saturation 99% while he was breathing ambient air. The patient was assigned to the nephrology department of this hospital for treatment.

The patient was diagnosed with hypertension for 20 years and was treated with “Nifedipine Controlled Release Tablets 30 mg bid and Benazepril 10 mg bid”, and the blood pressure was controlled at the level of 145/90 mmHg; type 2 diabetes was diagnosed for 5 years, and insulin “Humira 25R” was injected subcutaneously in the morning and evening, 8 U each. Coronary stenting was performed 1 year ago. The patient had a history of smoking and drinking for 30 years.

The results of blood routine, coagulation function, thyroid function, and myocardial enzyme spectrum were normal; anti-glomerular basement membrane (GBM) antibodies and anti-neutrophil cytoplasmic antibodies (ANCA) (including myeloperoxidase [MPO] and PR3) were detected by indirect immunofluorescence (IIF) and flexible Multi-Analyte Profiling (xMAP), respectively, and the results were negative. Other laboratory test results are shown in Table 1. We recommended further kidney morphological examinations to prepare for kidney biopsy. He rejected our suggestion and was discharged from this hospital to seek other drugs for the treatment of the disease.

Laboratory Data.

Variable* Reference Range October 25, 2019 April 2020 May 18, 2020 June 23, 2020
Blood Hb (g/L) 130–175 124 104 102
BUN (mmol/L) 2.2–8.2 11.5 11.61 13 26.9
SCr (μmol/L) 20–115 151 274 344 255
UA (μmol/L) 200–440 341 243 372 362
eGFR (mL/min/1.732) 45.734 22 16.901 24.272
TP (g/L) 60–85 64 48.5 45.8
ALB (g/L) 35–55 42.2 26.7 29.5
PTH (pg/mL) 15–65 39.1 96.9 17
CD4+ T cell (/μL) 550–1440 662 898.75 465
Urine Protein - 2+ 4+ 2+ 3+
A/Cr, mg/mmol 0–3 132 62.52 154.84
T/Cr (g/g) 0–0.2 2.2 1.1 3.08
24hTP (g) 0–0.15 3.16 2.86 10.52

Tests for hepatitis B surface antigens and surface antibodies, hepatitis C antibodies, antinuclear antibodies, anti–double-stranded DNA antibodies, plasma protein electrophoresis, urine protein-peripherin detection, anti-MPO antibody, anti-PR3 antibody, anti-GBM antibody and anti-PLA2R antibody were negative.

Hb, hemoglobin; BUN, blood urea nitrogen; SCr, serum creatinine; UA, uric acid; eGFR, estimated glomerular filtration rate; TP, total protein; ALB, albumin; PTH, parathyroid hormone; A/Cr, albumin/creatinine; T/Cr, total protein/creatinine; 24hTP, 24-hour urine total protein.

Second hospitalization (May 18, 2020)

The patient went to other institutions for examination 1 month ago. The results are shown in Table 1. He agreed to undergo a renal biopsy to confirm the pathological diagnosis. He had severe edema of both lower limbs. The antihypertensive drugs were adjusted to nifedipine controlled-release tablets and terazosin. Laboratory inspections are shown in Table 1. The volume of the left kidney was 123 mm × 60 mm × 56 mm, and the volume of the right kidney was 111 mm × 58 mm × 13 mm. Fundus examination revealed scattered hemorrhage and exudation of the retina, thin arteries, and increased reflection in both eyes. The pathological diagnosis of renal biopsy was nodular diabetic glomerulosclerosis with massive crescent formation (Figure 1). IgG was linearly deposited on the wall of renal tubule capillaries and part of basement membrane in immunofluorescence (staining intensity was 2+). We are considering active treatment of glomerular proliferative lesions and propose the following as treatment recommendations: methylprednisolone 8 mg tid, mycophenolate mofetil 0.5 g bid, glutathione and sulodexide.

Figure 1

Pathological results of light microscope. A total of 17 glomeruli under light microscope. Three globules are ischemic and sclerotic, and the mesangial cells and stroma of the remaining globules are moderately and severely proliferated, mainly with an increase in mesangial stroma. K-W nodules can be seen, basement membrane thickening, tumor-like expansion of peripheral capillary loops (A, B). Among them, four cell fibrous crescents, six fibrous crescents and one small cell fibrous crescent are seen (C, D). The renal interstitium is flaky mononuclear and lymphocyte infiltration accompanied by fibrosis (E, F). Staining method: A, B, E are PAS staining; C, D, F are PASM+MASSON staining. Magnification: A–D, 400×; E, F, 100×.

Third hospitalization (June 23, 2020)

Laboratory inspections are shown in Table 1.

Discussion

Edema is a common symptom of kidney disease, but it is not unique. We examined the patient and ruled out hypothyroidism (normal thyroid function), liver cirrhosis (normal liver function), deep vein thrombosis (no thrombosis in lower extremity venous color Doppler ultrasound), and cardiogenic edema (brain natriuretic peptide [BNP] 484.7 pg/mL). Provide evidence from the side to support that the cause of the patient's edema is likely to come from kidney disease. The patient had diabetes and hypertension for 5 years and 20 years, respectively. Fundus examination revealed scattered hemorrhage and exudation of the retina, thin arteries, and increased reflection in both eyes. It is considered that the fundus changes are caused by diabetes [5, 6]. In addition, the kidney ultrasound showed that the kidneys were normal and slightly larger, the capsules were smooth, and the renal vascular resistance was normal, Please check the format of this paragraph, it is different other paragraph. which did not conform to the manifestations of renal damage caused by hypertension. Therefore, it is preliminarily inferred that the patient is likely to have diabetic nephropathy.

Diabetic nephropathy is one of the main complications of diabetes. It is the manifestation of diabetic microangiopathy in the kidney and is also one of the important causes of end-stage renal disease [1, 2]. It is characterized by functional changes such as glomerular hyperfiltration and proteinuria and structural changes such as thickening of the glomerular basement membrane, mesangial matrix expansion, glomerulosclerosis, and arteriolar hyalinosis [3, 4]. In the patient's biopsy report, the typical features of diabetic nephropathy, such as K-W nodules, can be seen in the light microscope results. It is worth noting that there are massive crescent formations in the biopsy report of this patient, of which cell fibrous crescents accounted for 29.4% and fibrous crescents accounted for 35.3%, and immunofluorescence showed that IgG was deposited along the basement membrane. Crescent formation is the histopathologic hallmark of anti-GBM disease [7]. However, the negative anti-GBM antibody in laboratory tests can rule out combined anti-GBM nephropathy. Glomerular crescents are a prominent feature of rapidly progressive crescentic glomerulonephritis [8]. There have been individual reports of crescents in diabetic nephropathy [9, 10]. In this patient, in addition to glomerular disease, there is also another important aspect, namely severe renal interstitial disease. Drugs and infections are the most common causes of renal interstitial lesions. The patient has no history of infection at the initial stage of onset, but has used traditional Chinese medicine for several months before the second hospitalization, and the composition of the drug is not clear. We speculate that the application of drugs with unknown ingredients leads to renal interstitial disease, which is reflected in the increase in serum creatinine and increased urine protein. However, because the drugs are unknown, we cannot determine whether the formation of the crescent is related to them. Therefore, we use the antioxidant effect of glutathione to treat renal interstitial lesions, and considering that the crescents have developed to fibrosis, we use hormones combined with mycophenolate mofetil to treat the changes of the crescents.

Monitor and control of blood glucose and blood pressure are also essential for treatment. It is worth mentioning that when benazepril was initially used to control blood pressure, the serum creatinine was 160 mol/L. After the second hospitalization, the serum creatinine was 344 μmol/L. At this time, continued application of benazepril, an angiotensin converting enzyme inhibitors (ACEI)/angiotensin receptor blocker (ARB) antihypertensive drug, would aggravate the damage to the kidney, and so it was replaced with another type of antihypertensive drug.

After 1 month of treatment, the patient's serum creatinine level decreased, renal function recovered, and serum protein increased, but urine protein level increased. We consider that it is related to the progression of diabetic nephropathy and the remission of part of the crescent. The patient is still being followed up, and the treatment effect still needs further evaluation.

Conclusion

Early diagnosis of diabetic nephropathy is very important. In addition, it is necessary to avoid the application of drugs with unknown ingredients to avoid secondary damage to the kidney.

Figure 1

Pathological results of light microscope. A total of 17 glomeruli under light microscope. Three globules are ischemic and sclerotic, and the mesangial cells and stroma of the remaining globules are moderately and severely proliferated, mainly with an increase in mesangial stroma. K-W nodules can be seen, basement membrane thickening, tumor-like expansion of peripheral capillary loops (A, B). Among them, four cell fibrous crescents, six fibrous crescents and one small cell fibrous crescent are seen (C, D). The renal interstitium is flaky mononuclear and lymphocyte infiltration accompanied by fibrosis (E, F). Staining method: A, B, E are PAS staining; C, D, F are PASM+MASSON staining. Magnification: A–D, 400×; E, F, 100×.
Pathological results of light microscope. A total of 17 glomeruli under light microscope. Three globules are ischemic and sclerotic, and the mesangial cells and stroma of the remaining globules are moderately and severely proliferated, mainly with an increase in mesangial stroma. K-W nodules can be seen, basement membrane thickening, tumor-like expansion of peripheral capillary loops (A, B). Among them, four cell fibrous crescents, six fibrous crescents and one small cell fibrous crescent are seen (C, D). The renal interstitium is flaky mononuclear and lymphocyte infiltration accompanied by fibrosis (E, F). Staining method: A, B, E are PAS staining; C, D, F are PASM+MASSON staining. Magnification: A–D, 400×; E, F, 100×.

Laboratory Data.

Variable* Reference Range October 25, 2019 April 2020 May 18, 2020 June 23, 2020
Blood Hb (g/L) 130–175 124 104 102
BUN (mmol/L) 2.2–8.2 11.5 11.61 13 26.9
SCr (μmol/L) 20–115 151 274 344 255
UA (μmol/L) 200–440 341 243 372 362
eGFR (mL/min/1.732) 45.734 22 16.901 24.272
TP (g/L) 60–85 64 48.5 45.8
ALB (g/L) 35–55 42.2 26.7 29.5
PTH (pg/mL) 15–65 39.1 96.9 17
CD4+ T cell (/μL) 550–1440 662 898.75 465
Urine Protein - 2+ 4+ 2+ 3+
A/Cr, mg/mmol 0–3 132 62.52 154.84
T/Cr (g/g) 0–0.2 2.2 1.1 3.08
24hTP (g) 0–0.15 3.16 2.86 10.52

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