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Year : 2007  |  Volume : 17  |  Issue : 2  |  Page : 80-86

A case with paraplegia, urinary tract infection and renal failure


Correspondence Address:
Vivekanand Jha

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-4065.37029

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How to cite this article:
Jha V, Singh K, Varma S, Suri V, Das A. A case with paraplegia, urinary tract infection and renal failure. Indian J Nephrol 2007;17:80-6

How to cite this URL:
Jha V, Singh K, Varma S, Suri V, Das A. A case with paraplegia, urinary tract infection and renal failure. Indian J Nephrol [serial online] 2007 [cited 2023 Feb 5];17:80-6. Available from:

CPC Editor : Vivekanand Jha

CPC Chairman : Kartar Singh, Professor and Head of Gastroenterology

Clinical Incharge : Subhash Varma, Professor and Head of Internal Medicine

Clinical Discussant : Vikas Suri, Assistant Professor of Internal Medicine

Pathology Discussant : Ashim Das, Additional Professor of Histopathology

(This case was discussed as a staff clinical pathological exercise at PGIMER on 22 nd August 2007)

This 54-year-old male presented with fever and reduced urine output for the last one month and altered sensorium for 15 days. In the background, he had progressively worsening root pains in both the lower limbs for eight months for which he was evaluated by orthopedicians. An MRI revealed prolapsed intervertebral disk (PIVD) in the lumbar spine and epidural Inj. Depomedrol was given twice. Three days after the second injection, he developed sudden onset lower limb flaccid paralysis and an abscess at the site of the injection.

Fever was high-grade, intermittent, associated with chills and rigors and dry cough, no history of pyuria or hematuria. The urine output had gradually decreased over the last one month with oliguria for the last four days. The sensorium had been fluctuating with irrelevant talk, but there were no convulsions nor any upper limb weakness. There was no previous history of any chronic disease. He had taken desi medication for back pain.

On examination, he was drowsy but agitated. The BP was 115/80 mm of Hg, pulse rate 120/min and RR 30/min. He had a left corneal ulcer, was dehydrated, had a bedsore. There was no lymphadenopathy and bilateral edema feet was present. The heart sounds were normal and there were no additional sounds. Respiratory examination showed normal vesicular breathing, with no added sounds. There was no neck rigidity, tone was decreased in lower limbs, power was Grade 4/5 in upper and 0/5 in lower limbs. Reflexes were 2+ in upper and absent in lower limbs with B/L mute plantars. The pupils were normal. Abdomen was soft with tenderness in the epigastrium region, liver was 4 cm below the right costal margin, spleen 2 cm below left costal margin.

Imaging studies

USG abdomen: Right Kidney 10.9 cm; left kidney 11.1 cm. Both had a smooth outline, increased cortical echoenicity, an indistinct C/M differentiation. There were renal calculi and dilated left ureter. Compression USG showed no evidence of femoropopliteal DVT. The X-ray chest was normal. The CT KUB showed bilateral nephrolithiasis, Lt nephrocalcinosis/ureteric calculus and bilateral pleural effusion.

The spinal MRI revealed the lumbar spine to be essentially normal in outline and curvature. There was loss of T2 hyperintensity involving all the lumber disks suggestive of disk desiccation; mild chronic disk bulges were noted at L4-5 and L5-S1 levels. Mild effacement of the fat in the neural foramen region along with small annular tears were also present. The thecal sac was normal in outline and the cauda equina roots were evenly spaced. There was no evidence of any obvious thickening, distortion or displacement that may indirectly indicate underlying arachnoiditis.

The MR imaging of the brain revealed hyperintense signals involving both mastoids, suggestive of mastoiditis; fluid was noted in bilateral ethmoid and sphenoid sinuses suggestive of sinusitis. The brainstem and basal ganglia were essentially normal. Multifocal punctate hyperintense areas were seen in the frontal and the parietal regions, some were in the periventricular location while others extended to the subcortical white matter. Diffusion weighted images suggested active lesions, either demyelinating or acute ischemic lesions.

The NCCT abdomen revealed bilateral pleural effusion and enlarged liver and spleen. Kidneys were normal in size but showed globular outline suggestive of an underlying renal parenchymal disease. A hyperintense focus was noted in the right kidney suggestive of a calculus, along with tiny hyperdense foci in the medulla of the left kidney suggestive of medullary calcinosis. The left ureter was mildly dilated and had a hyperdense focus in its course suggestive of a ureteric calculus. There was subtle stranding of the perinephric pad and the thickening of renal fascia. The bladder was empty and there was a curvilinear calcification along the posterior aspect of the Foley's catheter.

The radiological impression was that of degenerative disk disease with diffuse disk bulges at L4-L5 and L5 -S1;T2 hyperintense multifocal lesions which could represent acute demyelinating lesions or small infarcts which are acute or embolic, hepatosplenomegaly, mild ascitis, bilateral pleural effusion, acute renal parenchymal disease with left medullary calcinosis. There was right nephrolithiasis and left ureterolithiasis and vesical calcification.

Course and Management: He was managed as acute renal failure, secondary catheter-related urosepsis. He received IV antibiotics along with CVP-guided fluids. A possibility of iatrogenic arachnoiditis was considered for his paraplegia. On Day 5 of the hospital stay, in view of worsening encephalopathy, renal functions, pleuropericardial rub and persistent acidosis, peritoneal dialysis was given. The patient developed intractable hypotension and subsequent cardiorespiratory arrest from which he could not be revived.

Unit Diagnosis: Lower motor neurone type paraplegia with bowel and bladder involvement (spinal shock)??Iatrogenic arachnoiditis. B/LNephrolithiasis/UTI with urosepsis with acute renal failure/DIC/encephalopathy (? uremic ??/ CNS infarcts)

Vikas Suri

I would like to discuss this patient's illness in three phases: the first phase when he had a lumbar disk disease and paraplegia, the next one was when he presented with fever, renal failure and nephrolithiasis and the final one that led to the demise of this patient.

What is the evidence of lumbar disk disease? He had root pains, a positive SLR test and MRI evidence of lumbar disk disease. Radiculopathy is approximately 95% sensitive for some processes that affect the nerve roots including PIVD. Why did he develop paraplegia? Transient paraparesis is known after epidural drug instillation due to inflammation of spinal root, generally this transient paraparesis improves within 4-6 h. Other causes could be intra-cord injection. This is unlikely as chances of cord injection are very low with caudal route. The MRI did not show any evidence of transverse myelitis, epidural abscess or hematoma. There have been case reports of intra arterial injection of the drug leading to acute onset paraplegia developing within hours, but this patient had paraplegia after 72 h of the epidural injection. Arachnoiditis due to polyethyl glycol preservative is a known complication of epidural drug instillation. The clinical symptoms of back pain, sensory symptoms and paraplegia are consistent with this etiology. I cannot rule out an underlying infection. A study showed that arachnoiditis, bacterial meningitis and conus medullaris syndrome developed after epidural injection. This patient also had altered sensorium which developed side by side. A study published in JAMA in 2003 revealed five patients who developed altered sensorium after epidural injection of depomedrol due to a rare fungus, Exophiala.

The current presentation included fever, UTI, encephalopathy and renal failure. In spite of the presence of a short history and normal size kidneys, I cannot go away from a diagnosis of underlying chronic kidney disease as my patient had anemia, hyperphosphatemia, low to normal calcium, hyperuricemia and history of chronic analgesic and desi medication use. So I think this patient had acute renal failure over preexisting chronic kidney disease. Fever could have been due to bed sore; a possibility of infective endocarditis is suggested by splenomegaly and septic infarct in the brain. However, the cardiac examination and ECG were normal. The UTI is likely as there were pus cells in urine along with risk factors (paraplegia, prolonged catheterization, nephrolithiasis). The sterile urine culture can be explained by multiple antibiotic administration before coming to PGI. Infection with fungal and unusual organisms including resistant UTI with Gram-negative bacteria can develop in the presence of obstruction (stones), underlying immunosuppression and renal failure. Another important feature was the sudden deterioration in renal functions. His creatinine at admission was 3.8 mg/dl but rose to 8.05 mg/dl within four days. One should consider renal papillary necrosis if renal function rapidly deteriorates. Tuberculosis is suggested by anemia, high ESR, thrombocytopenia, sterile pyuria, hepatosplenomegaly and ascites but the normal chest X-ray argues against this. The CT KUB had no sign suggestive of renal tuberculosis and I do not have urine AFB.

Is it sarcoidosis? Points in favor again are anemia, increased ESR thrombocytopenia, hyperuricemia and hepatosplenomegaly. Points against are normal chest X-ray, absence of lymphadenopathy and normal calcium. A word about renal sarcoidosis: it is rare, various studies have shown incidence of 1-22% but everybody should / will agree that normal X-ray and an ACE level do not exclude sarcoidosis. Hypercalciuria is the most common renal manifestation and is a risk factor for nephrolithiasis.

How can I explain the normal calcium in this patient? In a previous CPC at PGI, a 35-year-old male had presented with renal failure, hyperuricemia, hyperphosphatemia, hypercalcemia, bilateral nephrolithiasis, left side nephrocalcinosis and autopsy revealed sarcoidosis with widespread metastatic calcification, suggesting that renal failure can rarely be the initial manifestation of sarcoidosis and normal calcium does not rule it out.

Is it tumor lysis syndrome? It is defined as a combination of hyperuricemia, hyperphosphatemia, hypocalcemia, hyperkalemia, acidosis with renal failure secondary to destruction of a large number of neoplastic cells. But where is the malignancy? Most often this is due to a hematological malignancy. However, none of the biochemical, hematological or my radiological investigations point to any specific malignancy causing the syndrome but I cannot rule out an occult malignancy.

The cause for encephalopathy was multifactorial. Preterminally he had sepsis resulting in DIC. I consider a possibility of pulmonary embolism as he was bedridden and could not be given heparin because of thrombocytopenia and epistaxis.

Dr Suri's diagnosis


?Occult malignancy with tumor lysis syndrome

Complicated urinary tract infection

Sepsis, disseminated intravascular coagulation

S Varma: During the patient's life we discussed whether we can have one diagnosis for the total presentation or whether this patient had more than one problem. At least one problem (PIVD) was entirely different. He had renal stone as well as nephrocalcinosis and then he had problems related to sepsis. For hepatosplenomegaly, anemia, albuminuria and hypoproteinemia we considered malignancy, viz. lymphoreticular disease. There are not enough indicators of infective endocarditis.

Dheeraj Gupta, Additional Professor of Pulmonary Medicine: Whenever one is in a difficulty to knit up multi-system involvement, systemic vasculitis should always be considered. This can explain all the manifestations such as the central hyperdensities in the MRI, renal failure, hepatosplenomegaly, anemia and epistaxis.

Sanjay Jain, Professor of Internal Medicine: This patient does give a history of chronic analgesic abuse and in that situation papillary necrosis may not be a result of only infection but can be part of analgesic intake.

  Pathology Protocol Top

Ashim Das, Additional Professor of Histopathology

A partial autopsy was performed on this individual. The peritoneal cavity yielded 1.5 liters and each pleural cavity contained around 400 ml of straw-colored fluid.

Both kidneys together weighed 370 g. The outer surface showed extensive hemorrhagic areas involving both the cortex and medulla; the right more than the left [Figure - 1]. The cut surface showed multiple tiny abscesses in the renal parenchyma. Numerous tiny soft yellowish stones filling the whole of pelvis, both ureters and bladder were also seen [Figure - 2].

Microscopy revealed extensive proliferation of atypical lymphoid cells in the peritubular capillaries and medullary vessels. The glomerular capillaries showed occasional atypical cells. These cells were large with moderate cytoplasm and having a prominent nucleolus [Figure - 3],[Figure - 4],[Figure - 5],[Figure - 6],[Figure - 7]. In addition, multiple neutrophilic abscesses were also seen in the renal parenchyma, occasionally destroying the glomeruli [Figure - 8]. The atypical cells are CD20+ve but CD3-ve. Occasional cells in the interstitium, but not those in the vessels were myeloperoxidase positive [Figure - 9]. This constellation of findings was consistent with a diagnosis of angiotropic/intravascular large B cell lymphoma with coexisting pyelonephritis

A fleshy mass was seen in the mesentery with no other lymph node enlargement. Microscopy revealed a large collection of atypical lymphoid cells; either indicating an extranodal proliferation of lymphoid cells or localized involvement of lymph nodes. No other lymph nodes were seen to be involved by this process.

Spleen weighed 456 g. The sinuses of red pulp showed extensive collection of atypical lymphoid cells. The bone marrow was normocellular with adequate representation of hemopoietic cells. No atypical cells were seen [Figure - 10].

Both lungs together weighed 950 g. These were heavy with a solitary thrombus in the pulmonary artery. The inter-alveolar capillaries showed collection of similar atypical cells with evidence of pulmonary edema [Figure - 11].

Skeletal muscle and myocardial capillaries showed collection of atypical lymphoid cells [Figure - 12].

Final Autopsy Diagnosis

  1. Angiotropic/Intravascular large B cell lymphoma involving both kidneys, spinal vessels, lungs, spleen and mesentery.
  2. Acute pyelonephritis with abscess formation in the renal parenchyma in a setting of bilateral nephrolithiasis.

Intravascular lymphoma (IVL) is defined as the intravascular proliferation of clonal lymphocytes with little to no involvement of the organ parenchyma and is a unique subset of diffuse large B-cell lymphoma (DLBCL). It is characteristically confined to intravascular spaces like venules, capillaries and arterioles but not large arteries and veins. Some people call it a "neoplasm of homeless lymphocytes", cells who forget to come out or have lost the power to transmigrate the vascular wall. There are different theories for this phenomenon. These cells are localized to extranodal organs like the kidneys, lungs, brain, spinal cord, skin and other organs, just like in this case. Lymph nodes, spleen and bone marrow are generally spared, as was seen this morning.

The commonest clinical presentation is neurological, with progressive multifocal cerebrovascular events, spinal cord and nerve root vascular syndromes, subacute encephalopathy and peripheral and cranial neuropathies. About one-third patients present with urosepsis. We could not examine the spinal cord here and hence can't see the pathology, but the clinical syndrome is quite consistent.

Aberrant expression of CD11a and CD49d (VLA-4) on IVL cells has been proposed as a possible mechanism because these adhesion molecules would enable tumor cells to home to cells that bear CD54 (CD11a ligand) and CD106 (CD49d ligand). Typically these cells are endothelial cells. The IVL cells are consistently lacking in CD29 (b1 integrin) and CD54 (ICAM-1), both of which are regarded as essential for lymphocyte homing and transvascular migration.

V Jha, Additional Professor of Nephrology: One feature of this case which carried the discussion in one direction was the presence of stones. This patient was on catheter for eight months and these could be infection-related calculi, simply because of prolonged catheterization. The renal failure was not related to obstruction but due to involvement with the lymphoma and secondly obviously with the urosepsis.

KS Chugh, Emeritus Professor of Nephrology: Indeed it is a unique case. I was thinking of the implications for future cases whether we can really have some kind of parameters by which we could look into and think of some conditions. In certain situations wherever there is lymphocytic infiltration in the kidney, urinary examination does help. I am not sure whether there would be a lymphocyturia in such a situation. Is it a possibility and whether examination could lead to some kind of diagnosis? I am not so sure that's why I'm asking this question whether this could be a parameter for future cases. Biopsy would have been very difficult to think of in such a situation particularly in a paraplegic individual with evidence of infection stones. In such a situation you do not think of renal biopsy.

S Varma: This diagnosis is very difficult to suspect and sometimes skin biopsy can be done. Since it is intravascular, it is unlikely that any urinary examination will show up the lymphomatous cells.

A Rajwanshi, Professor of Cytopathology: Cytological examination of urine will not pick up these because they are intravascular and not thrown out in the urine. But of course, if it is suspected on sonography, needle aspiration cytology can definitely help.

Pankaj Malhotra, Assistant Professor of Medicine: The bone marrow can, rarely, be involved in this process. At least one study has shown bone marrow involvement and the lymphoma cells were present in the vessels of the bone marrow and you can make a diagnosis on bone marrow examination if you see the cells have infiltrated into the vessels and are not otherwise interstitial or not in regular aggregates.


  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11], [Figure - 12]

  [Table - 1], [Table - 2]


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