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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2002  |  Volume : 13  |  Issue : 2  |  Page : 176-180
Missed Renal Infarction Presenting as the Nephrotic Syndrome: A Case Report


1 Department of Medicine, Division of Nephrology, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia
2 Department of Radiology, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia
3 Department of Surgery, Division of Cardio-thoracic Surgery, King Khalid University Hospital, College of Medicine, King Saud University, Riyadh, Saudi Arabia

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   Abstract 

Aortic dissection may be associated with renal disease. The presentation, especially in the later stages of the process, includes proteinuria, hematuria and impairment of renal function. Thus the clinical picture may be confused with glomerulonephritis or hypertension. We present a case of ischemic nephropathy resulting from involvement of the right kidney by an aortic dissection. The pateint presented with the nephrotic syndrome some two and a half months after the probable time when the aortic disection had occurred. At that time the initial back and flank pains had disappeared. Ultrasound examination revealed a smaller right kidney, compared to the left one. Imaging techneques, initaited for suspected renal artery stenosis, revealed aortic dissection involving the right renal artery starting from the descending aorta, distal to the origin of the left subclavian artery and extending down to the right common iliac artery; occluding the right renal artery. The medical literature is reviewed for patients presenting with ischemic nephropathy and the mechanisms of proteinuria discussed. We conclude that ischemic nephropathy can clinically mimic glomerulonephritis and can be missed if it is not included in the differential diagnosis of patients who present with heavy proteinuria and hypertension.

Keywords: Ischemic nephropathy, Dissection, Hypertension, Proteinuria.

How to cite this article:
Tarif N, Mitwalli AH, Al-Wakeel JS, Patel PC, Al-Smayer SA, Najm HK, Qudsi A, Abu-Aisha H. Missed Renal Infarction Presenting as the Nephrotic Syndrome: A Case Report. Saudi J Kidney Dis Transpl 2002;13:176-80

How to cite this URL:
Tarif N, Mitwalli AH, Al-Wakeel JS, Patel PC, Al-Smayer SA, Najm HK, Qudsi A, Abu-Aisha H. Missed Renal Infarction Presenting as the Nephrotic Syndrome: A Case Report. Saudi J Kidney Dis Transpl [serial online] 2002 [cited 2022 Aug 7];13:176-80. Available from: https://www.sjkdt.org/text.asp?2002/13/2/176/33131

   Introduction Top


Occlusion of the renal artery leads to the development of hypertension and in many cases proteinuria. [1],[2],[3],[4] This may confuse the attending physician as to the cause of hypertension. We here present a case of occlusion of the right renal artery, as a result of aortic dissection, presenting as hypertension, hematuria, nephrotic range proteinuria and renal impairment.


   Case Report Top


41-year-old Sudanese male with no significant past medical history presented to a local hospital complaining of severe interscapular back pain along with right abdominal and left flank pain. He was found to be hypertensive, had right lower abdominal and bilateral flank tenderness.

The initial investigations revealed raised serum creatinine of 209 µmol/L (2.38 mg/dl) and mildly raised liver enzymes. Urinalysis showed RBCs 15-25/HPF, WBCs of 3­5/HPF and Protein dipstick +3. A 24-hour urine protein excretion was 1.84 grams. Ultrasound of the abdomen showed normal liver and kidney echotexture; however size of the right kidney was 9.2 x 4.4 cm and left 10.8 x 4.8 cm. Intravenous pyelogram was reported as normal.

The patient's blood pressure peaked initially to 210 systolic and diastolic of 110 mm Hg and was treated with a calcium channel blocker (Amlodipine). Two and half months after initial presentation, he was referred to our hospital for evaluation of glomerulonephritis and was seen in the primary care clinic.

Repeated laboratory work-up revealed serum creatinine of 206 µmol/L (2.34 mg/dl). 24-hour urine protein excretion was 4.0 gram and urinalysis showed significant hematuria with RBC of 70/HPF, and WBC 4-8/HPF. Investigations for secondary causes of glomerulonephritis were negative. The patient was referred to the nephrology clinic for hypertension, renal impairment and proteinuria. He did not have any abdominal pain or back pain and was admitted for renal biopsy. Ultrasound revealed a small right kidney that was 7.4 x 3.0 cm and left kidney 11.0 x 5.0 cm. Radionuclide renal scan showed non­functioning right kidney.

The blood pressure was difficult to control with the atenolol 100 mg/day, amlodipine 10 mg/day and the diueretic, furosemide. 24-hour urine protein excretion remained 4.5 grams even with the control of blood pressure to < 160/95 mm Hg.

Magnetic Resonance Imaging (MRI) was requested to evaluate the presence of renal artery stenosis as a cause of hypertension. MRI revealed aortic dissection involving the right renal artery [Figure - 1]. A computed tomography (CT) scan also corroborated the presence of aortic dissection extending from the descending aorta distal to the origin of the left subclavian artery and extending to the right common iliac artery; occluding the right renal artery, [Figure - 2]. Angiogram confirmed the CT scan findings and showed leak in the thoracic part of the dissection [Figure - 3] a, b.

The patient's blood pressure was eventually controlled with the vasodilator, minoxidil and atenolol. He underwent graft replacement of the thoracic part of the dissection at another center and tolerated the surgery well.

On follow-up two months later, the blood pressure was controlled with atenolol and amlodipine. We decided not to intervene to correct the right renal artery dissection, since blood pressure was well controlled and renal function was stable (serum creatinine of 208 µmol/L (2.36 mg/dl) and proteinuria was +1.


   Discussion Top


Though it could be due to hypertension, the marked proteinuria in our patient was probably due to ischemic nephropathy. Poutasse in 1957 and others later, noted proteinuria with renal artery stenosis. [1],[2],[3]

Kumar and Shapiro [4] presented in 1980 three cases that had significant proteinuria of 1.0 to 12.9 grams per day secondary to renal artery stenosis. All three patients underwent nephrectomy of the stenosed side along with renal vein renin measurements. Proteinuria disappeared in two (follow-up one and 10 years) and in the third dropped from 9.0 grams to 1.0 gram after one month. They also documented drop in the level of renal vein renin levels after surgery.

Zimbler et al [5] reported their findings in 46 patients with renal artery stenosis. Cure of hypertension was noted with remission of proteinuria post angioplasty. They also noted that proteinuria was massive if the renal artery was completely occluded.

The pathophysiology of proteinuria induced by ischemia has been elucidated in animal models and humans.

Eisenbach et al [6] and Bohrer et al [7] infused renin and angiotensin II (AgII), respectively, and induced reversible proteinuria in the experimental animals. More recently, Miller et al [8] and Johnson et al [9] illustrated the development of focal segmental glomerulo­sclerosis and changes in the podocytes in rats after the infusion of AgII for 8 and 2 weeks, respectively.

Kimura et al [10] studied patients with unila­teral renal artery stenosis by catheterizing the ureters. They calculated glomerular capillary pressure and glomerular filtration rate using Para-amino hippurate and inulin infusions. Glomerular hypertension and hyper­filtration were noted in the non-stenosed kidney.

Alkhunaizi and Chapman, [11] recently reported a patient with unilateral renal artery stenosis who underwent renal biopsy of both kidneys. The ischemic kidney had normal glomeruli with hyperplasia of the juxtaglomerular apparatus and the contralateral kidney revealed focal segmental glomerulosclerosis (FSGS). Thus, the evidence suggests that it is probably the high AgII level that leads to glomerular proteinuria. The surge of AgII from the ischemic kidney may cause traction and detachment of podocytes from the base­ment membrane in the contralateral kidney forming a nidus of sclerosis that results in FSGS. [12] The high AgII level also affects efferent arteriole in the ischemic kidney that may exert physical pressure on the podocytes and may lead to sclerosis causing proteinuria. [13]

We believe that our patient had significant proteinuria due to ischemic nephropathy although renal biopsy was not done. Post operation follow-up of the patient showed stable mild impairment of renal function, easily controlled blood pressure with only two anti­hypertensive drugs, and diminution of proteinuria.

Another interesting observation in our patient was the decrease in renal size from 9.2 cm to 7.4 cm in a mater of two and a half months. Strandness et al [14] have shown, in their prospective follow-up of 54 patients with documented renal artery stenosis, a decrease in renal size by more than one centimeter in three (5%) patients by six months and in 14 (27%) patients by two years. They also found that in the ischemic kidney the size decreased more quickly with complete occlusion, severely elevated blood pressure and in the presence of bilateral ischemia. Our patient had complete occlusion of the right renal artery and his blood pressure was not well controlled initially, which most likely lead to the rapid decrease in the renal size. We conclude that ischemic nephropathy can clinically mimic glomerulonephritis and it can be missed if it is not included in the differential diagnosis of patients who present with heavy proteinuria.

 
   References Top

1.Poutasse EF. Occlusion of a renal artery as a cause of hypertension. Circulation 1956; 13:37-48.  Back to cited text no. 1  [PUBMED]  
2.Pasternack A, Eklund J, Krohn K. Renal artery stenosis and the nephrotic syndrome. Acta Med Scand 1967;181:265-8.  Back to cited text no. 2  [PUBMED]  
3.Montoliu J, Botey A, Torras A, Darnell A, Revert L. Renin induced massive proteinuria in man. Clin Nephrol 1979;11:267-71.  Back to cited text no. 3  [PUBMED]  
4.Kumar A, Shapiro AP. Proteinuria and nephrotic syndrome induced by renin in patients with renal artery stenosis. Arch Intern Med 1980;140:1631-4.  Back to cited text no. 4  [PUBMED]  
5.Zimbler MS, Pickering TG, Sos TA, Laragh JH. Proteinuria in renovascular hyper­tension and the effects of renal angioplasty. Am J Cardiol 1987;59:406-8.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Eisenbach GM, Liew JB, Boylan JW, Manz N, Muir P. Effect of Angiotensin on the filtration of protein in the rat kidney: a micropuncture study. Kidney Int 1975; 8:80-7.  Back to cited text no. 6  [PUBMED]  
7.Bohrer MP, Deen WM, Robertson CR, Brenner BM. Mechanism of Angiotensin II-induced proteinuria in the rat. Am J Physiol 1977;233:F13-21.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Miller PL, Rennke HG, Meyer TW. Glomerular hypertrophy accelerates hyper­tensive glomerular injury in rats. Am J Physiol 1991;261:F459-65.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Johnson RJ, Alpers CE, Yoshimura A, et al. Renal injury from angiotensin II mediated hypertension. Hypertension 1992;19:464-74.  Back to cited text no. 9  [PUBMED]  
10.Kimura G, London GM, Safar ME, Kura­mochi M, Omae T. Glomerular hyperten­sion in renovascular hypertensive patients. Kidney Int 1991;39:966-72.  Back to cited text no. 10    
11.Alkhunaizi AM, Chapman A. Renal artery stenosis and unilateral focal and segmental glomerulosclerosis. Am J Kidney Dis 1997;29(6):936-41.  Back to cited text no. 11    
12.Kriz W, Elger M, Nagata M, et al. The role of podocytes in the development of glomerular sclerosis. Kidney Int Suppl 1994;45:S64-72.  Back to cited text no. 12  [PUBMED]  
13.Kriz W. Progressive renal failure-inability of podocytes to replicate and the conse­quences for development of glomerulo­sclerosis. Nephrol Dial Transpl 1996;11: 1738-42.  Back to cited text no. 13    
14.Strandness DE. Natural history of renal artery stenosis. Am J Kidney Dis 1994; 24(4):630-5.  Back to cited text no. 14    

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Correspondence Address:
Hassan Abu-Aisha
Department of Medicine (38), King Khalid University Hospital, P.O. Box 2925, Riyadh 11461
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


PMID: 17660658

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  [Figure - 1], [Figure - 2], [Figure - 3]



 

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    Abstract
    Introduction
    Case Report
    Discussion
    References
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