A call from a concerned GP

They have been treating an 86yo lady who is resident in a local nursing home.  She has known Stage 3 CKD, hypertension, peripheral vascular disease, eczema, osteoporosis and mild/moderate Alzheimer’s disease (which which she is usually independent in dressing and eating+drinking).  She has suffered from urinary tract infections in the past and these have been associated with worsening in her cognitive state.

Usual medications:  Bendroflumethiazide, Perindopril, Donepezil, Omeprazole, Alendronate (weekly), Calcichew-D3.

She was seen as a home visit 5 days ago due to increased confusion and reduced oral intake.  She appeared clinically dehydrated, pyrexial (38.2) and BP was 100/55.  Urine dipstick showed ++Blood, +Protein, +Nitrites, +Leukocytes.  An MSU was taken and she was started empirically on Trimethoprim.  U&Es taken at the time were available later that evening and showed worsened renal function (see below), at which point the nursing home was phoned and the thiazide diuretic and ACE inhibitor stopped.  She was reviewed this morning, and she was now apyrexial, her cognitive state was improved, and the nursing staff reported that her oral intake was now starting increase.  However despite this reported improvement, her renal function had deteriorated further.

Serial Blood tests     Urea  (mmol/L)  Creatinine(umol/L) Sodium            Potassium

GP 5 months ago             8.7                        133umol/L              136                        4.5
Initial consult                  20.6                        205umol/L              151                        5.4
Today                             22.3                        267umol/L              147                        5.7

Neither the GP nor the patients family were keen on admission, as the as been associated with worsened confusion and agitation in the past, but wonder if this is now necessary?

What would your management plan would be?  Where would the patient be best managed?.

Write your advice

 

Now read what the expert wrote

 This lady has acute kidney injury on a background of chronic kidney disease.

Urosepsis can cause renal dysfunction in its own right, particularly in the elderly and those with pre-existing CKD.  In this case the history and the elevation of serum sodium, urea and creatinine in the first set of U&Es suggests that the patient is significantly dehydrated.  It is unusual to see overt hypernatraemia unless some form of disability – in this case reduced cognition- prevents the patient from drinking in response to thirst.

Stopping the ACEi and thiazide was the appropriate course of action.  The use of trimethoprim will partially confound the interpretation of the 2nd set of U&Es, as it competitively inhibits renal tubular creatinine secretion, causing increases in serum creatinine of around 30% in patients with CKD, likely accounting for the apparent worsening in these lab results.

The potassium level does not mandate admission, and whilst there has been an improvement in the sodium level, there is still a water deficit and probable dehydration present.  My advice was not to admit to hospital, but to push oral fluids in the nursing home, repeating bloods at the end of the week once the course of trimethoprim had been discontinued- provided function did not continue to decline then this could be safely managed in the community.

 

Creatinine rise on losartan (18)

A 60 year old lady on losartan and simvastatin had bloods done 3 months ago which showed urea 5.4, creatinine 70 and eGFR 81.  Repeat bloods this week showed urea 5.0, creatinine 138 and eGFR 35.  I advised her to stop her losartan and rechecked it the following day and it improved to urea 5.4, creatinine 81 and eGFR 68.

I have advised her to stay off her losartan and aim to check her BP next week and will consider felodipine for her hypertension.

Do I need to do anything further to investigate this lady or should I just avoid ARBs and ACEi and treat her hypertension as required with felodipine?

What further information would you seek before giving your opinion?

See more of the history or available results?

She has a history of ischaemic heart disease and peripheral vascular disease.

No urine has yet been sent for protein quantification.

Now consider what advice you would give.

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Now read what the expert wrote

If this represents a doubling of serum creatinine with no other precipitant then this is suggestive of renal artery stenosis, particularly if she has vascular disease elsewhere.

On the other hand, if she was unwell when the creatinine rose then this may just be the combined effects of dehydration and losartan.

The key issue would be if the urine dipstick is positive for protein.  If she were to have proteinuria then one could argue the need for recommencing losartan again.  If she has proteinuria and creatinine rises again with losartan then it would be reasonable to refer her to the renal clinic.


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Hypertension, renovascular disease and ACEI (17)

This 65 year old lady has a history of resistant hypertension and renal artery stenosis.  She previously had angioplasty to the left renal artery in 1994 and 1997 and had a right renal artery stent inserted in 2002 for an ostial stenosis.  She has been maintained on antihypertensive treatment since, though good control has never been obtained.

 She was kept on lisinopril until she was admitted with a haematemesis 2 years ago.  Her lisinopril was stopped but reintroduced and titrated up to 10mg. Her potassium rose to 5.6 on repeated measurement and lisinopril was stopped.

 Blood pressure control remains poor with levels typically around 170-180 systolic.  Do you think it would be a good idea to give her a small dose of lisinopril again?

What further information would you seek before giving your opinion?

See more of the history or available results?

Her eGFR has slowly declined and is 43 at present and PCR is 117.

Now consider what advice you would give.

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Now read what the expert wrote

She was well on her previous ACEI & her baseline state hasn’t changed.  It was, and always is, approriate to stop her ACEI when she was critically unwell, but she is now well, hypertensive & proteinuric, so yes – give her the lisinopril back & watch and see what happens to her U&Es.  I would accept up to a 20% increase in creatinine and potassium up to 6.


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Optimising an ACEI (16)

An 83 year old woman attends the GP surgery for a blood pressure review.

Blood pressure has been high for a while (systolic ~160).  She was taking ramipril 1.25mg and diltiazem HCL 360 mg OD.  She had been taking bendrofluazide but this was stopped during a recent hospital admission due to hypokalaemia.   BP a couple of weeks ago is still very high with values of 218/93 and 200/100. Consequently, I initially increased her ramipril 10 days ago to 2.5mg OD.  Her BP this week is 210/78 and repeat U+Es were ok, so I increased the dose again to 5mg.

She is sytemically well other than for a recent altered bowel and mild weight loss for which she has been referred to colorectal.

I was planning to increase ramipril to 10mg as tolerated but I am not sure how quickly I should be increasing the dose.   I am concerned about her high BP and also concerned about increasing the dose too quickly due to her age.  I also wonder if she requires any further investigation in view of her significant proteinuria?

What further information would you seek before giving your opinion?

See more of the history or available results?

Urine  ACR 467 and PCR 259.  No haematuria.  Her eGFR is 50 and stable.

Now consider what advice you would give.

Write your advice


Now read what the expert wrote

You’re doing all that I’d do. The proteinuria level is technically above the recommended referral threshold (PCR 100), but at her age I’d be unlikely to go on to do a biopsy unless she was actually nephrotic or had deteriorating function.   In view of the proteinuria, maximising ACEi would be my first step too.   This can be done quickly (days to weeks) provided BP and renal f(x) are monitored.

 If her eGFR drifts down or there is an increase in proteinuria then it would be worth referring her to the renal clinic. That said, you can allow up to around a 20% rise in creatinine around the time of institution of ACE inhibition.


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ACEi causing a drop in GFR (10)

This 72 year old lady has a previous medical history of hypertension, gout (thought to be thiazide induced) and acute renal failure secondary to gastroenteritis (12 years ago). She is on allopurinol, atorvastatin & 30mg of lisinopril.

3 weeks ago, I noted her eGFR had fallen to 50, with potassium of 5.3. Her U&Es were normal 3 months previously.  The specimen was repeated a week later, and showed a drop in eGFR to 37, with a potassium of 5.5. I asked her to stop her ACEI immediately, which she did, with a eGFR back up to 55 a week later.  Subsequently she restarted her lisinopril again as she felt “headachy” without it.  Unsurprisingly her eGFR dropped again to 45 with a potassium of 5.4. I have taken her off her lisinopril and asked her not to restart it again.

During this whole episode she has been totally well. Her blood pressure today was 132/70 (though it had been higher than this previously), with a normal abdominal examination, no urinary symptoms at all, and no blood or protein in her urine (though it was strongly positive for nitrites so I have sent an MSSU).

Is it possible she has renal artery stenosis or is there another explanation for her drop in renal function? I have put her on amlodipine temporarily although I believe this delivered suboptimal BP control in the past. Should I undertake any investigations for this lady?

Now consider which one of these three options to go for: 

  1. Give Advice
  2. See in Outpatients non-urgently
  3. Send this patient to us now!

Write your advice

Now read what the expert wrote

The long-held belief that a rise in creatinine with an ACEi equals a renal artery stenosis has probably been overstated over the years. The answer is “yes” – she may have, but our renal blood flow is partly dependent on angiotensin and changes whenever we use an ACEi.

The main points are that;
a) Intervention to renal artery lesions are now discredited except for all the most severe ones, which she hasn’t got.
b) She is very well, her creatinine is normal, her eGFR is OKish for her age, urinalysis is normal and her BP is excellent.

I would do nothing more than you are currently doing. I would accept eGFRs in the 40+ – for her if stable, and I would treat her as a straightforward hypertensive.


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