{"id":10798,"date":"2026-01-08T06:06:07","date_gmt":"2026-01-08T06:06:07","guid":{"rendered":"https:\/\/www.kauveryhospital.com\/ima-journal\/?p=10798"},"modified":"2026-01-08T06:06:07","modified_gmt":"2026-01-08T06:06:07","slug":"mri-spectrum-of-atypical-pres-in-a-juvenile-nephronophthisis-patient-on-hemodialysis","status":"publish","type":"post","link":"https:\/\/www.kauveryhospital.com\/ima-journal\/ima-journal-january-2026\/mri-spectrum-of-atypical-pres-in-a-juvenile-nephronophthisis-patient-on-hemodialysis\/","title":{"rendered":"MRI Spectrum of Atypical PRES in a Juvenile Nephronophthisis Patient on Hemodialysis"},"content":{"rendered":"

[vc_section][vc_row][vc_column][vc_column_text]<\/p>\n

Introduction<\/h2>\n

Posterior Reversible Encephalopathy Syndrome (PRES) is a neurotoxic clinico-radiological condition characterized by acute neurological symptoms such as seizures, altered mental status, visual disturbances, and headache, accompanied by vasogenic edema predominantly affecting the parieto-occipital regions. Although initially described as posterior and reversible, PRES is now recognized to present with a wide anatomical spectrum, including atypical involvement of the frontal lobes, temporal lobes, deep gray nuclei, cerebellum, and brainstem. Conditions associated with hypertension, renal failure, immunosuppressive therapy, and fluid\u2013electrolyte imbalance predispose to the syndrome by disrupting cerebral autoregulation and causing endothelial injury.
\nJuvenile nephronophthisis\u2014a hereditary cystic kidney disorder leading to early-onset chronic kidney disease (CKD)\u2014contributes to severe metabolic derangements, uremic endothelial dysfunction, and early dependence on hemodialysis, all of which increase the susceptibility to PRES. Patients undergoing maintenance hemodialysis experience rapid shifts in blood pressure and osmolality, further impairing vascular autoregulation. Early recognition of PRES is essential because timely blood pressure control and metabolic correction typically result in complete clinical and radiological recovery, whereas delayed intervention may lead to irreversible ischemia or hemorrhage.<\/p>\n

Case<\/h2>\n

A 22-year-old male with systemic hypertension and CKD secondary to juvenile nephronophthisis, maintained on thrice-weekly hemodialysis, presented with a single generalized tonic\u2013clonic seizure and transient loss of consciousness. There was no prior history of seizures or neurological illness. On presentation, his blood pressure was markedly elevated. Immediate blood pressure control was initiated using intravenous labetalol, achieving gradual stabilization. The patient underwent two additional hemodialysis sessions during admission to optimize metabolic parameters and reduce uremic load. Antiepileptic therapy was commenced for seizure management.<\/p>\n

MRI brain revealed multifocal T2-weighted\/FLAIR hyperintense lesions involving the bilateral frontal and parietal lobes (asymmetric), right occipital lobe, and left temporal lobe. Additional hyperintensities were seen in the bilateral cerebellar hemispheres, left thalamus, pons, and medulla, representing widespread supratentorial and infratentorial involvement. Several lesions demonstrated high signal on diffusion-weighted imaging but preserved ADC values, indicating vasogenic edema characteristic of PRES. A few punctate susceptibility blooming foci in the left parietal region suggested microhemorrhages, a feature associated with severe or advanced PRES. Symmetrical T1 hyperintensities were noted in the bilateral basal ganglia, likely representing metabolic changes related to CKD, such as manganese deposition. MR angiography revealed normal intracranial arterial caliber and flow, with no evidence of stenosis, vasculitis, or occlusion.<\/p>\n

\"\"<\/figure>\n
\"\"<\/figure>\n
\"\"<\/figure>\n

Following blood pressure control, dialysis optimization, and initiation of antiepileptics, the patient exhibited progressive neurological recovery. He remained asymptomatic for 24 hours after stabilization and was subsequently discharged in stable condition, with instructions for strict blood pressure monitoring, dialysis compliance, and neurological follow-up.<\/p>\n

Discussion<\/h2>\n

The clinico-radiological constellation in this young CKD patient strongly supports the diagnosis of atypical PRES, which is increasingly recognized in individuals with renal impairment. While classical PRES preferentially affects the parieto-occipital regions, atypical PRES\u2014particularly in renal and hypertensive patients\u2014often demonstrates extensive involvement of the frontal and temporal cortices, cerebellum, deep gray nuclei, and brainstem. This broader spectrum reflects severe endothelial dysfunction and impaired autoregulatory capacity resulting from uncontrolled hypertension, uremia, and rapid hemodynamic shifts during dialysis.<\/p>\n

The imaging pattern of DWI hyperintensity with preserved ADC values is a hallmark of vasogenic edema and helps differentiate PRES from acute ischemic stroke, where ADC reduction is expected. The presence of microhemorrhages is increasingly recognized in PRES and correlates with the severity of endothelial injury. Basal ganglia T1 hyperintensity is a common metabolic finding in chronic dialysis patients and does not represent an acute pathology. The patient\u2019s significant clinical improvement following blood pressure control and metabolic optimization further supports the diagnosis, as PRES typically demonstrates rapid symptom resolution when appropriately managed.<\/p>\n

This case highlights the broad MRI spectrum of PRES, emphasizing that extensive or atypical involvement should not detract from the diagnosis in the appropriate clinical context. Early therapeutic intervention\u2014particularly blood pressure control and correction of uremia\u2014is crucial to prevent progression to cytotoxic edema, infarction, or irreversible neurological injury. Follow-up MRI is recommended to confirm radiological resolution.<\/p>\n

Conclusion<\/h2>\n

This case underscores the diverse MRI spectrum of atypical PRES in a young patient with juvenile nephronophthisis on hemodialysis. Multifocal supratentorial and infratentorial vasogenic edema, microhemorrhages, and rapid clinical recovery following blood pressure stabilization strongly support the diagnosis. Recognition of atypical patterns is essential, particularly in renal patients, as timely management ensures complete reversibility and prevents long-term neurological morbidity.<\/p>\n

References<\/h2>\n
    \n
  1. Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med<\/em>. 1996;334(8):494\u2013500.<\/li>\n
  2. Bartynski WS. Posterior reversible encephalopathy syndrome, part 1: fundamental imaging and clinical features. AJNR Am J Neuroradiol<\/em>. 2008;29(6):1036\u20131042.<\/li>\n
  3. Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol<\/em>. 2015;14(9):914\u2013925.<\/li>\n
  4. McKinney AM, Short J, Truwit CL, et al. Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings. AJR Am J Roentgenol<\/em>. 2007;189(4):904\u2013912.<\/li>\n
  5. Lee VH, Wijdicks EF, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol<\/em>. 2008;65 (2):205\u2013210.<\/li>\n
  6. Covarrubias DJ, Luetmer PH, Campeau NG. Posterior reversible encephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR images. AJNR Am J Neuroradiol<\/em>. 2002;23(6):1038\u20131048.<\/li>\n<\/ol>\n
    \n
    \"Dr.<\/div>\n
    \n

    Dr. Kanagasabai
    \nKauvery Hospital, Chennai.<\/a><\/b><\/p>\n<\/div>\n<\/div>\n

    \n
    \"\"<\/div>\n
    \n

    Dr. Manish Yadav
    \n    Kauvery Hospital, Chennai.<\/a><\/b><\/p>\n<\/div>\n<\/div>\n

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