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    Hey Guys;

    I am doing a case study and I can't figure out what is causing his proteinuria but no glycouria?

    Or is it a simple case of glomerular capsule (bowman's capsule) has been damaged and they are leaking though?

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    Q2(a)

    HISTORY:
    The presentation of weight loss, weakness and lethargy over a reasonably chronic period suggests a condition that has a slow progression, hence probably not vascular or neurological. The weight loss, lethargy and polyuria/nocturia together make a strong case for diabetes mellitus [which is later counted against by the absence of glycosuria], although diabetes insipidus needs to be considered, too.
    EXAMINATION:
    The high bp reading obviously implies a hypertensive condition; however, we must bear in mind that renal hypertension is the 2nd most common cause of raised bp after essential hypertension, (the latter accounts for over 95% of cases (so chicken and egg scenario)).

    Other conditions to be kept as possibilities in our "keep an open mind" approach at this stage would be:-

    a) bearing in mind the patient's age, a neoplasm, possibly hypernephroma [although the report does not mention pyrexia - this is one tumour that causes fever] or a pituitary tumour reducing ADH secretion paradoxically (there is no mention of any visual symptoms suggestive of visual field defects, so unlikely).
    b) The impotence suggests neuropathy, supporting diabetic neuropathy, but hypertension can also cause impotence,either by the acceleration of atherosclerosis [reducing penile blood flow] or as a side effect of therapy [although this patient is probably not on antihypertensive medication - drug history is not given].
    c) Hypertensive nephropathy (seeing the very high bp reading, although isolated)
    d) A rarer condition that might lead to proteinuria (=nephrotic syndrome) e.g. amyloidosis or multiple myeloma.

    INVESTIGATIONS:
    The hyponatraemia, hyperkalaemia, uraemia and high creatinine all support chronic renal failure, but our enigma is the cause of this. One would consider hyperparathyroidism as one cause of a high alkaline phosphatase level (which is categorized as an LFT [liver function test], but can be high in many other conditions including renal failure), but this is ruled out by the hypocalcaemia. The low bicarbonate implies an acidosis (also indirectly given away by the 2nd Q!), but this is a common finding in renal disease anyway.

    My impression, keeping things simple and considering common conditions first [and defo if you are not a medical student], would be hypertensive nephropathy culminating in chronic renal failure.

    I hope this helps!

    M (former medical student)

    PS Watch this space for Q2 (b)
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    CarsAreGood


    Hi,

    Have you given up on this Q? NEVER GIVE UP! A bit of feedback on my post would make my 15 minutes invested in it worthwhile!

    BTW, what car do you drive, OR what is your dream car? - I have a 1994 SL320 [+ a few others - I agree c your username !]

    M
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    (Original post by CarsAreGood)
    Hey Guys;

    I am doing a case study and I can't figure out what is causing his proteinuria but no glycouria?

    Or is it a simple case of glomerular capsule (bowman's capsule) has been damaged and they are leaking though?

    Name:  Question.PNG
Views: 6
Size:  38.9 KB
    As above, there is definitely evidence of chronic kidney disease (CKD). In CKD, the ability of the kidney to excrete things that we don't want is reduced. This means that the kidneys are less able to excrete potassium, urea, creatinine, acids, phosphate, etc. This is why potassium, urea and creatinine are elevated. Since the kidneys are less able to excrete acids, acid accumulates - some of this acid is buffered by bicarbonate why explains why the bicarbonate is low.

    In CKD, there is also a loss of the diurnal rhythm of urine excretion - urine excretion usually occurs in the day and less so at night, however this is lost in CKD and so patients may have nocturia.

    Calcium is low (hypocalcaemia) because remember that the kidney has endocrine functions as well as metabolic functions. These endocrine functions are involved in red blood cell production (by secreting EPO), vitamin D production, and the maintenance of blood pressure (via the secretion of renin and the renin-angiotensin-aldosterone system (RAAS)). The ability of the kidney to carry out these functions are reduced in CKD. The final step in the production of active vitamin D (calcitriol or 1,25-dihydroxyvitamin D) is the hydroxylation of inactive vitamin D (calcidiol or 25-hydroxyvitamin D) by the enzyme 1-α-hydroxylase in the proximal tubule. Also, in CKD there is an accumulation of phosphate (as the kidneys cannot clear it) which increases the secretion of FGF23. FGF23 inhibits the enzyme 1-α-hydroxylase and so less vitamin D is produced. Remember than vitamin D increases uptake of calcium and phopshate in the gut, and so low levels of vitamin D cause the low calcium levels. The high phosphate levels can also cause calcium phosphate to precipitate out in tissues, also contributing to the low calcium. This low calcium is then sensed by the parathyroid glands which in turn release more parathyroid hormone (PTH) - this is known as secondary hyperparathyroidism. PTH tries to increase the levels of calcium by increasing resorption in the kidney, increasing the absorption of calcium in the gut by increasing vitamin D synthesis, and increasing osteoclast activity causing calcium to be released from bone (bone resorption). Alkaline phosphatase is also elevated in secondary hyperparathyroidism.

    Finally, since the blood pressure is extremely high, it is likely to be caused by hypertensive nephropathy. Hypertension damages the glomerular filtration barrier as well as the kidney tubules which leads to proteinuria. There is no glycosuria as glycosuria is seen in diabetes mellitus.
 
 
 
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