The Story of Glomerular Injury

This is an extract taken from chapter 92 of "The Conscious Notebook" (full text here and table of contents here

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It has been long since June met Professor Joatmon in his limestone cave of holistic medicine full of stalactites and stalagmites. At present if you move these curtains you can spot June looking smart in that suit, standing on the pulpit with a laser pointer in her hand. From a lecturer she has quickly become an Assistant professor now, teaching in the Macchapucchare College of medical sciences, Nepal. She’s at the moment presenting a paper on preventing and managing glomerular diseases in the community. You can stay on if you’d like to view her presentation.

June starts off with, “May we have the first slide please?”

Slide 1. Macchapucchare teaching hospital, Pokhara, Nepal.

The first slide is a picture of Macchapucchare teaching hospital, Pokhara, Nepal where I live and work. To talk on renal diseases their impact and strategy for long-term solutions I am going to begin by relating a story, which has been synthesized from the stories of a number of our patients and doesn’t necessarily reflect any real life patient. Prem Bahadur Khadka (not his real name) is a 25 year old boy who hails from a remote village near Jumla, Nepal and had never seen a bus or car in his life before he left his village for higher studies.

Slide 2.

This is his village where the only means of travel was an airstrip apart from the other option of a few days of walking.

Slide 3. Professor Joatmon’s village.

Prem was intelligent and soon after he finished his 10^th grade exams he decided to leave his village for higher studies.

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Slide 4.

He came to Pokhara, enrolled in a good school and saw proper roads and vehicles for the first time.

Slide 5.

As he was a good student he got into engineering and after finishing his degree, arrived in US as a software analyst. However he felt miserable there as he kept missing his relations and his mother’s cooking (among other things). He was actually relieved when he got the pink slip and lost his job after the economic slowdown.

Slide 6.

He came back to his village (and his mothers cooking) but found that by now he couldn’t adjust with his brothers who knew more than him about farming and all his knowledge of software was of no use in the village (which didn’t even have a single computer).

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Slide 7.

While all this was happening to Prem our protagonist in his macrocosm, quite unknown to him or anybody else a major war had already started inside his kidney where his glomeruli were being attacked by a lot of inflammatory cells.

Slide 8. A cell in Prem Bahadur’s glomerulus.

This is a cartoon borrowed from Harrison’s principles of Internal Medicine, which shows in molecular detail the happenings inside a cell in Prem Bahadur’s glomerulus. You can see how the antigens are processed and finally parceled into an endosomal compartment containing the MHC class II molecule .The antigen settles down into the groove of the MHC and sets off a chain reaction stimulating a clonal proliferation of hordes of inflammatory T cells.

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Slide 9.

This is the strong inflammatory response inside Prem Bahadur’s glomerulus as a result of which we expect to see a lot of protein and RBCs in his urine (if only we could have examined it earlier). However Prem Bahadur didn’t notice anything wrong with his urine. His neighbors noticed him growing plump day by day and complimented him on this sign of prosperity. At first Prem Bahadur was also happy that he was getting fat but later noticed that he was unable to enjoy his mother’s cooking due to a feeling of extreme nausea. This too was ignored by him until one day he developed extreme breathlessness and had to be rushed to our hospital in Pokhara.

Slide 10. Our hospital in Pokhara.

This is a picture of our hospital on a stormy night. When I saw him in our casualty (for the first time) I found him gasping for breath, his lungs were full of crepitations which we quickly treated with Lasix and referred him to Katmandu for dialysis. At Katmandu they dialyzed him for fluid overload and a urine analysis subsequently showed 3+ proteins and plenty of RBCs suggesting acute glomerular injury. He was immediately treated with high dose steroids and a renal biopsy was done.

Slide 11. Renal biopsy.

The biopsy showed focal areas of glomeruli that were sclerosed in segments.

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The fire was too severe to be quenched with steroids and it was already too late to prevent Prem Bahadur’s kidney from blowing up in smoke.

Slide 12.

He received a few more dialysis from Kathmandu and spent whatever money he had earned over the past few months. His brothers came forward to donate their kidneys for transplantation but that would mean selling off their land and cattle to go to one of the hospitals in India and Prem Bahadur wasn’t keen on that. The next slide is a Haiku sequence, which was mailed to me by a friend right after 9/11.

Slide 13. Haiku sequence.

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The last I heard of him was through one of our medical students also from the same village. Prem was spending his last days in deathbed with his family praying for him daily and it would be a matter of days or months before death would take him.

Slide 14. Summary of the story of glomerular injury.

This is a summary of the story of glomerular injury taken from Harrison’s principles of Internal Medicine which describes how it’s initiated by breakdown of tolerance leading to reactivity of antibodies with planted glomerular antigens which in turn generates a chemical cytokine mediated response leading to proliferation of inflammatory cells and subsequent irreversible renal damage (in a substantial number of people).

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The key word here is tolerance and (next slide).

Slide 15.

Tolerance is fast becoming popular in transplantation research but we need tolerance urgently before the need for transplantation arises to save our native kidneys (before the inflammatory cells attack them). As much as we need tolerance to save this Earth before a full-fledged war breaks out. That is the problem of glomerular injury for we don’t really know why this breakdown of tolerance occurs. We don’t even know why hypertension or diabetes occur (for that matter). Our present strategy is only to control them in the hope of slowing the progression of renal disease.