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Table of Contents
SPECIAL FEATURE
Year : 2019  |  Volume : 8  |  Issue : 2  |  Page : 104-112

A 57-year-old man with altered sensorium and renal failure


1 Department of Cardiology, Sri Venkateswara Institute of Medical Sciences, Sri Padmavathi Medical College for Women, Tirupati, Andhra Pradesh, India
2 Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Sri Padmavathi Medical College for Women, Tirupati, Andhra Pradesh, India
3 Department of Pathology, Sri Venkateswara Institute of Medical Sciences, Sri Padmavathi Medical College for Women, Tirupati, Andhra Pradesh, India
4 Department of 4Opthalmology, Sri Venkateswara Institute of Medical Sciences, Sri Padmavathi Medical College for Women, Tirupati, Andhra Pradesh, India

Date of Web Publication11-Nov-2019

Correspondence Address:
R Ram
Professor and Head, Department of Nephrology, Sri Venkateswara Institute of Medical Sciences, Tirupati, Andhra Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCSR.JCSR_57_19

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How to cite this article:
Kumar Reddy S P, Manual MB, Alekhya B, Swyritha G, Amarendra M, Naveen K, Sunnesh A, Sameera N S, Praveen N, Kumar P, Rukumangadha N, Prayag A, Ram R, Rajasekhar D, Kumar V S. A 57-year-old man with altered sensorium and renal failure. J Clin Sci Res 2019;8:104-12

How to cite this URL:
Kumar Reddy S P, Manual MB, Alekhya B, Swyritha G, Amarendra M, Naveen K, Sunnesh A, Sameera N S, Praveen N, Kumar P, Rukumangadha N, Prayag A, Ram R, Rajasekhar D, Kumar V S. A 57-year-old man with altered sensorium and renal failure. J Clin Sci Res [serial online] 2019 [cited 2019 Dec 16];8:104-12. Available from: http://www.jcsr.co.in/text.asp?2019/8/2/104/270755



A 57-year-old man presented with a history of headache and altered sensorium for the past 4 days. The headache was bifrontal, moderate to severe, intermittent, associated with nausea and vomiting. The patient had two episodes of loss of consciousness and preceded by history of tonic posturing of all four limbs. The patient had a history of incoherent speech for 3 days and excessive daytime sleepiness. The patient had a history of reduced urine output for the past 4 days. The patient complained burning sensation of feet. There was no history of fever, abdomen pain, loose stools, breathlessness, chest pain, palpitation, paedal oedema, haematuria and excess frothing of urine. In the past history, he was a patient of chronic obstructive pulmonary disease for the past 10 years on inhalers. He was diagnosed hypertension and dyslipidaemia 2 months back. He had a history of right upper-limb weakness and slurring of speech 2 months back. Magnetic resonance imaging (MRI) and magnetic resonance angiography of the brain showed the left internal carotid artery (ICA) watershed infarct with ICA stenosis. Digital subtraction angiogram showed 80% stenosis of left cervical ICA by irregular calcific plaque. Subsequently, he underwent ICA stenting. He was non-diabetic. He had no vices.

On general examination, he had no oedema, icterus, cyanosis, clubbing, koilonychia and lymphadenopathy. Pallor was present. Pulse: 80 bpm, normal volume, regular, all peripheral pulses equally felt, no radio-femoral delay, blood pressure: 180/100 mmHg, respiratory rate: 16/min and temperature: 98.4°F.

In the nervous system, the patient was conscious, disoriented to time place and person, facial deviation to the right side with sparing of the upper part of the face. The remaining cranial nerves were normal. Motor system: power 4/5 in all four limbs. Deep tendon reflexes: 2+ in all four limbs. Right plantar reflex: Up going. Left plantar: normal response. Sensory systems were normal. There were no cerebellar signs or signs of meningitis. Skull and spine were normal. There is no peripheral nerve thickening.

On cardiovascular system examination, apex beat is in the fifth left intercostal space, half-an-inch medial to midclavicular line, normal cardiac resonance, normal first and second heart sounds and no added sounds.

On respiratory system examination, trachea central, no flattening or bulges on chest wall, both sides of chest moving equally with respiration, resonant note on percussion all over the chest, vocal resonance is normal and equal on both sides, normal vesicular breath sounds, no crackles/rhonchi and no pleural rub heard.

In the abdomen, all quadrants move equal with respiration, no palpable organomegaly, no free fluid and bowel sounds present.

The investigations of the patient are given in [Table 1]. The patient was initiated on haemodialysis. During hospital stay, the anorexia had progressively worsened, nausea increased and he consumed less and less quantities. He also developed waxing and waning of sensorium levels. There was no improvement of urine output even after 45 days of regular haemodialysis. He died due to sudden cardiac arrest.
Table 1: Laboratory Investigations

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  Differential Diagnosis Top


Headache and altered sensorium of 4-day duration were the first complaints of the patient. The differential diagnosis of altered sensorium is listed in [Table 2].
Table 2: Differential diagnosis of altered sensorium

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The majority of causes could be excluded for the lack of history or clinical features. Such causes include drugs and alcohol, infections, shock, trauma, intracranial structural causes, hypertensive encephalopathy, intracranial haemorrhage, hypoxia, hypoglycaemia and hyperglycaemia, hepatic encephalopathy and hypercalcaemia. The investigations revealed that the patient had hyponatraemia and renal failure.

The causes of hyponatraemia fall into three groups: hyperosmolar hyponatraemia, euosmolar hyponatraemia and hypoosmolar hyponatraemia. The hypoosmolar hyponatraemia has two categories: impaired capacity of renal water excretion and excessive water intake. The list of causes of hyponatraemia, are listed in [Table 3].
Table 3: Case of hyponatraemia

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The cause of hyponatraemia that is obvious from the list is the hyponatraemia due to acute or chronic renal failure.

Hyponatraemia can occur only with advanced acute or chronic renal failure. In these patients, free water excretion is mainly limited by the reduced glomerular filtration rate. As an example, when the glomerular filtration rate is at 10 mL/min (14 L/day) with approximately 20% of filtrate reaching the diluting segments of the nephron, the maximum electrolyte-free water generation is approximately 2.8 L/day. In advanced renal failure, the minimum urine osmolality can be 200–250 mOsm/kg H2O despite appropriate suppression of arginine vasopressin secretion; thus, unrestricted water intake might lead to hyponatraemia. The higher minimum urine osmolality is due to increased solute excretion per functioning nephron resulting in osmotic diuresis.

The patient had raise in serum creatinine (SCr) from 1.2 mg/dL to 9.2 mg/dL in 2-month interval.

In clinical medicine, physicians encounter patients who present with progressive renal impairment of seemingly unknown aetiology. The duration of disease is brief or may even be undefined. These patients are neither acute kidney injury nor chronic kidney disease (CKD) (previously called chronic renal failure). On ultrasonography of the kidneys, this group of patients has normal-sized kidneys, while the presence of small contracted echogenic kidneys establishes the diagnosis of CKD. This group encompasses is heterogeneous set of clinical syndromes. The list includes acute interstitial nephritis, bilateral renal vein thrombosis (RVT), multiple myeloma, thrombotic microangiopathy, malignant hypertension, scleroderma crisis, sarcoidosis, toxaemia and atheroembolic disease.[1],[2] In addition to this list, as the patient had been subjected to contrast dye-based study, contrast-induced nephropathy (CIN) should also be included.

CIN is defined as the impairment of renal function – measured as either a 25% increase in SCr from baseline or a 0.5 mg/dL (44 μmol/L) increase in absolute SCr value – within 48–72 h after intravenous contrast administration.[3]

For renal insufficiency to be attributable to contrast administration, it should be acute, usually occurring within 2–3 days (although it has been suggested that renal insufficiency developing up to 7 days post-contrast administration should be considered CIN); it should also not be attributable to any other identifiable cause of renal failure. A temporal link is thus implied.[4] Following contrast exposure, serum creatinine levels peak between 2 and 5 days and usually return to normal in 14 days.

In the above list of causes, acute interstitial nephritis is an immune-mediated disorder commonly drug induced. Patients present with fever, rash and eosinophilia. The urine may contain white blood cells and white cell casts. Eosinophiluria is present in up to 80%–85% of patients.[5]

Although RVT has numerous aetiologies, it occurs most commonly in patients with nephrotic syndrome (i.e., >3 g/day protein loss in the urine, hypoalbuminaemia, hypercholesterolaemia and oedema). Other diseases or situations that have been associated with RVT include antithrombin III deficiency, protein C or S deficiency, antiphospholipid antibody syndrome,[6],[7],[8] pregnancy or oestrogen therapy, renal vein invasion by malignant cells, post-renal transplantation, Behcet's syndrome and extrinsic compression (e.g., lymph nodes, tumour, retroperitoneal fibrosis and aortic aneurysm). Aside from renal cell carcinoma, the other associations are uncommon. Trauma, ingestion of oral contraceptive agents, dehydration (infants) and steroid administration also have been associated with RVT. RVT is an uncommon but definite problem in neonates.[9],[10] A possible association exists between RVT and the Factor V Leiden mutation in this age group.

Neither the history nor the clinical features nor the investigations are suggestive of multiple myeloma, thrombotic microangiopathy, malignant hypertension, systemic sclerosis and sarcoidosis. The remaining cause is atheroembolic disease which merits discussion. Because atheroembolisation is ubiquitous, atheroembolic renal disease can mimic several different clinical syndromes. Knowledge of the risk factors and recognition of the variable clinical presentations can heighten the likelihood of making a diagnosis. The typical patient at risk is a man older than age 60 years with known atherosclerotic disease presenting with a clinical triad of a precipitating event, acute or subacute renal failure and typical skin findings. The presence of eosinophilia should raise the level of suspicion. Our patient was a 57-year-old man who underwent ICA stent placement following which there was raise in SCr over 2-month interval. Unlike the CIN, the atheroembolic acute kidney injury is frequently irreversible.[11] Our patient also had no improvement of renal function. In addition, the MRI brain had shown new onset of lacunar infects that were not reported before ICA stent placement.

Osler is quoted as saying 'It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has.' This is underscored by the presentation reported herein. The absence of typical triad and also the skin lesions of the atheroembolic disease made the clinical diagnosis of challenging. This patient presentation illustrates the importance of considering the diagnosis of atheroembolic disease in any elderly patient with progressive kidney disease of unknown cause. The presentation also underscores the importance of performing a renal biopsy for definite diagnosis. I would also like to know the reports of serum complement levels and findings of fundus examination.

The diagnosis is atheroembolic disease, with multiple organ involvement, could it possible, when seemingly only an atheroma in ICA was disturbed during stent placement?

The ICA is reached through the femoral artery and aorta. The severity of atherosclerosis in these arteries accounts for the degree of atheroembolism. Mechanical trauma has a key role. Guidewires and catheters can scrape aortic walls and disrupt atherosclerotic plaques.


  Ophthalmologist Diagnosis Top


We examined the fundus of the patient. The fundus revealed Hollenhorst plaques [Figure 1]. Hollenhorst plaques refer to yellow, orange refractile cholesterol emboli which occur at retinal arteriole bifurcations arising from carotid or aortic arch atheromatous disease.
Figure 1: Hollenhorst plaques

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Independently, Hollenhorst[12] and German investigators, Witmer and Schmid,[13] described these retinal plaques in 1958. Hollenhorst's later work established the clinical significance of the plaques as markers of cerebrovascular disease[14] and increased mortality.[15] His observations and experimental work demonstrated that the plaques contained cholesterol.[16]

Hollenhorst plaques tend to originate from carotid arteries or the aorta. This finding is consistent with atherosclerotic lesions in carotid arteries. The initial assumption is that a Hollenhorst plaque originates from the stenosed, ipsilateral ICA. The ophthalmic artery is the first branch of the ICA, which then leads into the central retinal artery (CRA).[17],[18] This direct anatomical route between ICA and CRA supports this assumption.

Hollenhorst plaques serve as markers of past emboli events but are poor predictors of future events. These plaques may or may not cause an Retinal artery occlusion (RAO). The discovery of asymptomatic emboli has a greater concern for a patient's systemic health than visual health.

Unless a Hollenhorst plaque completely obstructs a vessel causing an RAO, no ocular treatment is necessary. All patients with retinal emboli should be referred to the patient's primary care provider for bilateral carotid duplex.

Differential diagnosis of retinal emboli includes the following:[19][i] Calcific emboli: white, dull (non-refractile), due to their larger size typically found in the CRA close to the optic disc. This finding is consistent with cardiac disease originating from heart valve calcifications; [ii] Platelet-fibrin emboli: white/grey, dull (non-refractile), elongated. This can be a finding for both cardiac and carotid diseases; however, cholesterol emboli are more common in carotid disease; [iii] Talc emboli: small, white/yellow, highly refractile, typically located in the macular region. This finding is associated with intravenous drug abuse; [iv] Lipid/fat emboli: usually cannot visualise the emboli, cotton wool spots are often seen. This finding is associated with long bone fractures and chest trauma, i.e., Purtscher retinopathy; [v] Tumour cells: these proliferative neoplastic cells which can fall off the main lesion and lodge in the retinal arterioles and [vi] Septic emboli: these deposits are associated with bacterial endocarditis.


  Pathologist's Diagnosis Top


Much has been learnt from animal experiments in which cholesterol crystals were injected into the renal artery followed by serial observations of the vascular lesions. Cholesterol crystals are often too small and irregularly shaped to completely obstruct the artery in which they lodge, thus causing secondary ischaemic atrophy rather than an acute renal infarction. Shortly after lodging, neutrophils and eosinophils infiltrate the affected arterioles. In time, the ensuing foreign body endothelial inflammatory reaction causes intimal proliferation, giant cell formation and chronic fibrosis, narrowing of the vascular lumen over weeks to months in a stepwise pattern.

Because the crystals are insoluble in body fluids and not removable by phagocytosis, they persist indefinitely. Histologically, cholesterol crystal emboli are identified as biconvex, needle-shaped and empty clefts, referred to as cholesterol cleft because they dissolve during formalin fixation. However, when specimens are snap frozen with liquid nitrogen and the frozen specimen is examined under polarised light, the birefringent character of the cholesterol crystals may be seen. Crystals are mostly found in the lumen of arcuate and interlobular arteries. Rarely, small crystals lodge in the afferent arterioles and glomerular capillaries.

Vessel recanalization of chronic lesions can occur. Global and segmental sclerosis of glomeruli may be present. In cases of massive cholesterol emboli, zonal areas of tubular necrosis may occur. Immunofluorescence microscopy: no specific staining is seen. Electron microscopy: extensive foot process effacement may be present.[20]


  Final Diagnosis Top


The diagnosis of the discussant, even when some information was withheld, is spot on. Unbeknownst to the discussant is the presence of the skin lesions. The patient had 'blue toes' [Figure 2]. Blue toe syndrome is due to the tissue ischaemia secondary to cholesterol crystal or atheroembolisation. Serum complement levels of this patient were low – C3: 13.5 mg/dL (reference range: 84–193 mg/dL) and C4: 2.1 mg/dL (reference range: 20–40 mg/dL). The presence of the biconvex, needle-shaped and empty clefts in glomeruli on renal biopsy is indeed finding a 'needle in haystack'.
Figure 2: Photomicrography showing Intraglomerular cholesterol clefts (a) (Haematoxylin and eosin, ×40), Clinical photograph showing blue toe syndrome (b)

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Atheroembolic renal disease is the Cinderella of nephrology in that often Cinderella (the patient and their clinical findings) and her shoe (the final diagnosis of atheroembolic disease) are not matched in life.[21] It is a silent masquerader.[22] Some of the features such as livedo reticularis, purpuric rash, severe hypertension, hypocomplementaemia, raised erythrocyte sedimentation rate, eosinophilia or eosinophiluria and even a necrotising glomerulonephritis may force an alternative diagnosis.

The renal function in atheroembolic disease is affected acutely, subacutely, or in a chronic but slow, progressive way.[23],[24],[25],[26],[27],[28],[29] [Table 4] describes each of these presentations.[30]
Table 4: Presentations of atheroembolic disease[30]

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The reason that atheroembolic disease is difficult to diagnose is that it may be missed on histology, even if suspected. The reasons are as follows: [i] The cholesterol emboli do not uniformly affect the renal arteries.[33] The affected areas should be in the biopsy specimen for the diagnosis to be made: [ii]The cholesterol crystals may embed only in the arcuate vessels,[34] and the downstream changes seen will be those of non-specific ischaemia. In such condition, cutting multiple sections of the biopsy may on occasions reveal the diagnostic cholesterol cleft, which would be otherwise missed: [iii] Cholesterol crystals are mostly found in the lumen of arcuate and interlobular arteries. However, the renal biopsy avoids medulla; [iv] Sometimes, the cholesterol embolisation may only be evident in sections stained with special stains and not in the initial serial sections stained with haematoxylin and eosin. For that, all the tissues submitted for histology are examined. This includes the frozen tissue submitted for immunofluorescence microscopy[35] and the tissue submitted for resin embedding. The latter should always be examined by semi-thin microscopy stained with toluidine blue, whether electron microscopy is performed or not, and some authors suggest that this is more effective than paraffin sections[36] in demonstrating the lesions.

There is consensus that atherosclerosis is a pre-requisite for the occurrence of atheroembolic disease. The risk factors and 'trigger' events for atheroembolism are given in [Table 5]. However, 4%–69% of patients had atheroembolism spontaneously.[30]
Table 5: Risk factors and ‘trigger’ events[22],[30]

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Atheroembolic disease is a multisystem disease, and clinical features can be varied. Multifocal lesions and progressive tissue loss secondary to ischaemic injury involve the kidney, skin, brain, myocardium and intestines. The clinical manifestations are described in [Table 6]. There is no definitive treatment.[30] The treatment strategies are given in [Table 7].
Table 6: Clinical manifestations of atheroembolic disease[30]

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Table 7: Treatment strategies

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After confirmation of the diagnosis, the patient was initiated on prednisolone 0.3 mg/kg/day and atorvastatin 20 mg/day. He was also initiated haemodialysis. Although dietary guidance was given, he had progressive worsened malnutrition and expired after 45 days.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
de Wardener HE, Del Greco F. The influence of solute excretion rate on the production of a hypotonic urine in man. Clin Sci 1955;14:715-23.  Back to cited text no. 1
    
2.
Brady HR, O' Meara YM, Brenner BM. The major glomerulopathies. In: Braunwald E, Hauser SL, Fauci AS, Longo DL, K, Jameson LJ, Hasper DL, editors. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw Hill; 2011. p. 1580-90.  Back to cited text no. 2
    
3.
Kellum JA, Lameire N, Aspelin P, Barsoum RS, Burdmann EA, Goldstein SL, et al. Guideline for the KDIGO work group. Kidney disease: Improving global outcomes.KDIGO clinical practice guideline for acute kidney injury. Kidney Int 2012;2:1-138.  Back to cited text no. 3
    
4.
Murphy SW, Barrett BJ, Parfrey PS. Contrast nephropathy. J Am Soc Nephrol 2000;11:177-82.  Back to cited text no. 4
    
5.
Palmer BF. Nephrotoxicity of nonsteroidal antiinflammatory agents, analgesics, and inhibitors of the renin-angiotensin system. In: Coffman TM, Molitoris BA, Falk RJ, Neilson EG, Schrier RW, editors. Diseases of the Kidney & Urinary tract. 7th ed. Philadelphia, USA: Lippincott Williams & Wilkins; 2013. p. 943-58.  Back to cited text no. 5
    
6.
de Azevedo FV, Maia DG, de Carvalho JF, Rodrigues CE. Renal involvement in antiphospholipid syndrome. Rheumatol Int 2018;38:1777-89.  Back to cited text no. 6
    
7.
El Zorkany K, Bridson JM, Sharma A, Halawa A. Transplant renal vein thrombosis. Exp Clin Transplant 2017;15:123-9.  Back to cited text no. 7
    
8.
de Freitas RA, de Lima ML, Mazzali M. Early vascular thrombosis after kidney transplantation: Can we predict patients at risk? Transplant Proc 2017;49:817-20.  Back to cited text no. 8
    
9.
Bidadi B, Nageswara Rao AA, Kaur D, Khan SP, Rodriguez V. Neonatal renal vein thrombosis: Role of anticoagulation and thrombolysis – An institutional review. Pediatr Hematol Oncol 2016;33:59-66.  Back to cited text no. 9
    
10.
Niada F, Tabin R, Kayemba-Kay's S. Spontaneous neonatal renal vein thromboses: Should we treat them all? A report of five cases and a literature review. Pediatr Neonatol 2018;59:281-7.  Back to cited text no. 10
    
11.
Brady HR, Brenner BM. Acute renal failure. In: Kasper DL, Braunwald E, Fauci AS, Hauser SL, Longo DL, Jameson JL, editors. Harrison's Principles of Internal Medicine 16th ed. New York: McGraw-Hill Education; 2005.  Back to cited text no. 11
    
12.
Hollenhorst RW. Ocular manifestations of insufficiency or thrombosis of the internal carotid artery. Trans Am Ophthalmol Soc 1958;56:474-506.  Back to cited text no. 12
    
13.
Witmer R, Schmid A. Cholesterin crystal as a retinal arterial embolus. Ophthalmologica 1958;135:432-3.  Back to cited text no. 13
    
14.
Hollenhorst RW. Significance of bright plaques in the retinal arterioles. JAMA 1961;178:23-9.  Back to cited text no. 14
    
15.
Hollenhorst RW. Vascular status of patients who have cholesterol emboli in the retina. Am J Ophthalmol 1966;61:1159-65.  Back to cited text no. 15
    
16.
Hollenhorst RW, Lensink ER, Whisnant JP. Experimental embolization of the retinal arterioles. Trans Am Ophthalmol Soc 1962;60:316-34.  Back to cited text no. 16
    
17.
Lawlor M. Bakri et al.: Is carotid ultrasound necessary in the evaluation of the asymptomatic Hollenhorst plaque? (Ophthalmology 2013;120:2747-8). Ophthalmology 2014;121:e49-50.  Back to cited text no. 17
    
18.
Bakri SJ, Luqman A, Pathik B, Chandrasekaran K. Is carotid ultrasound necessary in the evaluation of the asymptomatic Hollenhorst plaque? Ophthalmology 2013;120:2747-80.  Back to cited text no. 18
    
19.
Kaufman EJ, Patel BC. Hollenhorst plaque. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470445/. [Last updated on 2018 Nov 24].  Back to cited text no. 19
    
20.
Lusco MA, Najafian B, Alpers CE, Fogo AB. AJKD atlas of renal pathology: Cholesterol emboli. Am J Kidney Dis 2016;67:e23-4.  Back to cited text no. 20
    
21.
Scoble JE, O'Donnell PJ. Renal atheroembolic disease: The Cinderella of nephrology? Nephrol Dial Transplant 1996;11:1516-7.  Back to cited text no. 21
    
22.
Mittal BV, Alexander MP, Rennke HG, Singh AK. Atheroembolic renal disease: A silent masquerader. Kidney Int 2008;73:126-30.  Back to cited text no. 22
    
23.
Thadhani RI, Camargo CA Jr., Xavier RJ, Fang LS, Bazari H. Atheroembolic renal failure after invasive procedures. Natural history based on 52 histologically proven cases. Medicine (Baltimore) 1995;74:350-8.  Back to cited text no. 23
    
24.
Mayo RR, Swartz RD. Redefining the incidence of clinically detectable atheroembolism. Am J Med 1996;100:524-9.  Back to cited text no. 24
    
25.
Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis 1999;33:840-50.  Back to cited text no. 25
    
26.
Scolari F, Tardanico R, Zani R, Pola A, Viola BF, Movilli E, et al. Cholesterol crystal embolism: A recognizable cause of renal disease. Am J Kidney Dis 2000;36:1089-109.  Back to cited text no. 26
    
27.
Scolari F, Ravani P, Pola A, Guerini S, Zubani R, Movilli E, et al. Predictors of renal and patient outcomes in atheroembolic renal disease: A prospective study. J Am Soc Nephrol 2003;14:1584-90.  Back to cited text no. 27
    
28.
Meyrier A. Cholesterol crystal embolism: Diagnosis and treatment. Kidney Int 2006;69:1308-12.  Back to cited text no. 28
    
29.
Modi KS, Rao VK. Atheroembolic renal disease. J Am Soc Nephrol 2001;12:1781-7.  Back to cited text no. 29
    
30.
Scolari F, Ravani P. Atheroembolic renal disease. Lancet 2010;375:1650-60.  Back to cited text no. 30
    
31.
Frock J, Bierman M, Hammeke M, Reyes A. Atheroembolic renal disease: Experience with 22 patients. Nebr Med J 1994;79:317-21.  Back to cited text no. 31
    
32.
Zucchelli P, Zuccalà A. The diagnostic dilemma of hypertensive nephrosclerosis: The nephrologist's view. Am J Kidney Dis 1993;21:87-91.  Back to cited text no. 32
    
33.
Flory CM. Arterial occlusions produced by emboli from eroded aortic atheromatous plaques. Am J Pathol 1945;21:549-65.  Back to cited text no. 33
    
34.
Hannedouche T, Godin M, Courtois H, Ducastelle T, Delpech A, Tayot J, et al. Necrotizing glomerulonephritis and renal cholesterol embolization. Nephron 1986;42:271-2.  Back to cited text no. 34
    
35.
Handler FP. Clinical and pathologic significance of atheromatous embolization, with emphasis on an etiology of renal hypertension. Am J Med 1956;20:366-73.  Back to cited text no. 35
    
36.
Jones DB, Iannaccone PM. Atheromatous emboli in renal biopsies. An ultrastructural study. Am J Pathol 1975;78:261-76.  Back to cited text no. 36
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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