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?.

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 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.

 

A 44 year old man with previous interstitial nephritis (22)

This man was diagnosed with interstitial nephritis secondary to mesalazine (prescribed for ulcerative colitis) in 2009.  His eGFR has remained stable since and is curently 42.  Last year he was started on lisinopril for hypertension but this was stopped some months later as his BP was too low.  The plan then was to reintroduce if BP over 130/80 or if proteinuria worsened.  Urinary PCR was 15 mg/mmol.

His PCR has increased a bit to 20; blood pressure on his last two visits 123/83, 124/96.  I just wanted to check that we should add in lisinopril 2.5mg in vew of this.

I also note that his cholesterol was recently 6.1, LDL 4.2, chol/HDL ratio 4.2.  I wonder if we should be starting a statin also?  He has no significant family history of heart disease and is an ex-smoker.  Other therapy is azathioprine (only) for ulcerative colitis.

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That level of proteinuria, just outside the normal range, wouldn’t trigger me in his case.  Any threshold is going to be arbitrary, but 50 is sometimes uesd.  Consistently over 50 maybe.  His BP is well within limits. His CV risk is low (see Further Info)

Proteinuria is in general a strong marker for progression of renal disease, with higher levels indicating much higher risk.  Mostly we are talking about glomerular leaking of protein.  He actually had tubulointerstitial disease rather than glomerular, which is associated iwth lower levels of proteinuria in general, and lower risk of progression if the cause is removed (as it is in him).

If he showed any signs of long term deterioration I’d be stricter but he seems to have experience a small fall in creatinine over the last couple of years.

Further info

  • CV risk calculator gives him a 10y risk of CV events of 3.6% – this does not include proteinuria however, which would ‘usually’ probably at least double risk, though this is contentious in this patient’s unusual circumstances.
  • Interstitial nephritis (Edren Textbook)
  • The Edrep Glomerulonephritis page has a link to a 10 min lecture on Interstitial nephritis (requires Flash).  The Resources page there has more links

Anaemia, heart failure and CKD (21)

This elderly man has multiple medical problems.  His main current problem is heart failure – he has moderate LV dysfunction, valvular heart disease and pulmonary hypertension.  He is seen by the Heart Failure Nurse and we have reached the point where we agree his treatment is palliative.  He gets recurrent peripheral oedema and ascites.  His renal function shows a urea of around 20 and creatinine of around 200.  At home he is able to walk with a frame from his bedroom to the living room but this makes him breathless.  He is a type 2 diabetic and also has mild memory impairment.

He has had a chronic long standing anaemia over a number of years.  This has seen his haemoglobin slide from the 10.3 down to 8.3 when last checked.   He had GI investigations and was found to have a number of polyps and an area of angiodysplasia.  He has had a couple of transfusions.  It was decided earlier this year that further investigation was not appropriate.  He is on iron so it is difficult to know how much of his anaemia is due to his renal problems.

When discharged last week it was suggested that we should contact you about erythropoietin treatment.  Improvement of his anaemia might help his heart failure a little though I suspect this would only be temporary.  He is very frail and clinic attendance might not be possible.  I would be grateful for your advice

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Current medications include: bumetanide 5mg OD, metolazone 2.5mg once weekly and insulin.

 

 

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There are 2 issues here:

1. Anaemia & EPO – the advice given to you is a bit misleading.  EPO is designed to bring haemoglobin up slowly, the recommended rise being 1gm/month.  In other words, he’s going to get decent haemoglobin in about 2-3 months time.  Furthermore, EPO is contraindicated in GI bleeding and his anaemia is probably mainly due to angiodysplasia rather than renal disease.  I would normally commit someone like this to regular transfusion.

2. Oedema – I would try and dry him out and ignore his U&Es.  Our ability to control heart failure is so often hampered by our worrying about the urea rising but I would ignore it.

 

 

 


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Anaemia and CKD III (20)

This diabetic lady has CKD3 with microalbuminuria of 14.8.  She was recently seen in the haematology clinic regarding her chronic anaemia (most recent haemoglobin was 100g/l).  She was in hospital at the end of last year when she was transfused and started on oral iron.  At that time endoscopy was normal but she has previously had angiodysplasia.  Haematology felt this is most likely anaemia of chronic disease rather than iron deficiency anaemia, and that it probably relates to her deteriorating renal function.  Her most recent eGFR was 52, creatinine 91 and urea 8.6.  They have suggested that she might be a candidate for EPO injections to boost her blood count.  I wonder if I should be referring her to renal clinic?

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B12 and folate are normal.  Ferritin 85, Transferrin saturations 17%

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Renal anaemia with a GFR above 30ml/min is extremely unusual indeed.  10% of anaemia in CKD 3 is explained by EPO-deficiency, but the patients involved are in the eGFR of 30-35 bracket, rather than 52 as in this case.  Given the history of previous angiodysplasia this is most likely the explanation for the recurrent anaemia.


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Anaemia and CKD in the frail elderly (19)

This rather frail 85 year old man has recently become anaemic.  His haemoglobin has dropped down to around 9.0 having previously been around the 11 mark.  Haematinics are normal.  His latest renal function shows urea 15.6, creatinine 213, potassium 4.8 and eGFR 26.

His general health is poor.  He lives at home and is slowly mobile with a zimmer but has had falls and is awaiting a residential or nursing home placement.

Can we attribute his anaemia to his CKD and should he be considered for EPO?  Or should we refer him to haematology for further assessment of his anaemia?

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Co-morbidities include: recent significant stroke, diabetes, angina, Parkinson’s disease, atrial fibrillation, hypertension and LVF.

 Currently: ACR 155, PCR 260, Ferritin 60.

12 months ago: Hb 10.5, urea 11.4, creatinine 168, ACR 120, PCR 185

3 years ago: ACR 35

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This gentleman has evidence of progressive CKD – now Stage 4 – almost certainly secondary to diabetic nephropathy given the longstanding albuminuria and proteinuria.  His anaemia has been evident for some time.  His haematinics do indicate that he may be Fe deficient – his ferritin is only 60 (we would normally look for a minimum of 100). His iron saturation has not been done but should be >20%.   I would suggest in the first instance repeat of his iron stores specifically to include iron saturation and ferritin.  If they are below targets then I would suggest oral iron supplementation.

 I don’t think there is a good indication for a renal clinic referral, but he may be a candidate for erythropoietin therapy if he remains anaemic when iron stores are replete.

 

 


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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?

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

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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?

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

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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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Drop in GFR in Alcohol Dependence (8)

This 78 year old man has a medical history complicated by previous alcoholic dependence, alcoholic cardiomyopathy, recurrent bouts of atrial fibrillation and flutter.  He also suffers from hypertension, Vit.B12 deficiency and hypothyroidism.

Up to now his kidney function has remained quite stable with his last normal blood result in 8 months ago. On routine kidney screening last month there was a marked deterioration in his kidney function with eGFR dropping to 39 and ACR 7.5.  There was no obvious cause for this but the patient did admit to drinking most of a bottle of wine per day and described slight dehydration and mild metallic taste in his mouth.

On discussion he agreed to cut alcohol out, drink more fluids, and we stopped his Bendroflumethiazide and reduced his Enalapril to 10mgs. Repeat U&E shows little change in his function and I would appreciate your advice as to his further assessment.

I am unsure whether he needs referral to yourselves in view of his sudden deterioration without obvious cause, or whether it would be worthwhile monitoring this further and arranging an USS in the community?

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Current medication; Bendroflumethiazide, Folic acid, Atorvastatin, Amiodarone, Levothyroxine, Enalapril, Hydroxocobalamin, Paracetamol.

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It’s a little bit difficult to know with this one; he’s complicated with quite a few things going on. In the first instance, I’d give him time. If he was dehydrated on a full dose of enalapril plus a diuretic he may have some tubular necrosis that may take time to heal; he may also have done some irreversible damage.

I don’t think there’s anything else to do at the moment. I’d be tempted to maximise his enalapril back up again if reducing it hasn’t had any effect – he needs it for his cardiomyopathy. Repeat his bloods in another month or so – if better, great, and if stable, then he’s got enough renal function to survive on. If he’s worse then perhaps we should see him, given everything that’s going on with him.

I wouldn’t rush to scan unless you’ve get any other reason to – haematuria, suprapubic mass, urinary symptoms etc; we do many scans and get back little in the way of positive results. If he’s worse again then that becomes more important.


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Gout Prevention in CKD (12)

Please advise on dose titration of allopurinol and gout management in this 62 year old man with CKD3 and multiple medical problems. He recently developed gout with a urate of 0.86. His CKD is stable, with eGFRs usually between 30-40 (latest eGFR 33).

I have given colchicine but pain is persistent and urate still very high.

Past medical history includes; Cor pulmonale, Type 2 Diabetes, COPD, AF, Morbid obesity (BMI 52).

He can attend clinics – would you recommend a medical or renal referral?


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Current Medications; Metformin, Gliclazide, Digoxin, Lisinopril (5mg), Warfarin, Amiodarone, Furosemide (250mg/day)

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I have always thought that response to colchicine is almost useful as a diagnostic test; if he’s getting pain despite colchicine, is it really gout or is it another condition in conjunction with a high urate?

As for allopurinol, start when inflammation has subsided at 100mg / day. In CKD it is recommended to start low dose and titrate dose till urate <.35. Check urea and urate every few weeks.

If we are sure this is gout, and if colchicine is not settling his pain, he could have a short course of steroids‚ something like 5 days of prednisolone (20mg OD), but that may play up with his diabetes.

Does he need to be seen in clinic? – possibly and almost certainly if this problem becomes more complex. If gout control is difficult, rheumatology might be best first stop. His renal function is not deteriorating.

2 further thoughts;
1. He is close to the point where metformin is contra-indicated, in which case he may need to get into the diabetic clinic for advice on insulin
2. He is on a huge dose of furosemide which will undoubtedly push his urate up. If he has cor-pulmonale, I would expect him to have some peripheral oedema because of his right-ventricular pressures. If he is free of peripheral fluid, and especially if his BP is low or low-normal. I would cut his diuretic back a bit, allow him to gain some fluid in order to see what happens.


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Anaemia in CKD (11)

This fairly fit 83 year old lady with a history of hypertension usually has an eGFR around 40.  She is on lisinopril 10mg and furosemide 40mg (best tolerated combination, bendroflumethiazide did not have any effect on blood pressure) and her BP is well controlled on this combination at around 130/68 at her latest visit.

For several months she has had a haemoglobin of around 106 g/l.  Her haematinics and blood indices are otherwise normal apart from a slightly low haematocrit of 0.32.

Is an eGFR of around 40 low enough to cause renal anaemia?  She is only a little tired, are we best just to monitor things?  Should I be looking for another cause for her anaemia?

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That haemoglobin is a little low for that eGFR, but it may be that you find no other cause. There is a big range of Hb values at any eGFR, including at end stage.

It is unusual to drop below 100g/l until eGFR is substantially less than 30, but she isn’t below 100. This level of renal impairment could be compounding another cause and look for deficiencies of haematinics and check a CRP as an indicator of inflammation.

Interestingly ACEi do worsen renal anaemia slightly. However the effect isn’t huge, if this is the best combination for her, she might prefer to tolerate the slightly lower Hb.  Her current level of Hb is above the level at which guidelines would recommend commencing EPO therapy.


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