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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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?

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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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Incidental Discovery of Stage 4 CKD (9)

This 87 year old man has had a marked deterioration in his renal function.  6 years ago urea was 9.6 and creatinine 168.  Routine blood tests 2 weeks ago revealed urea 12.2, creatinine 244 and eGFR 22.  He has no symptoms and is feeling well. 

He does have a history of prostate problems and is currently awaiting urology assessment regarding symptoms of BPH. 

On examination pulse 70, BP 145/80, heart sounds 1+2, no peripheral or sacral oedema, chest clear with fine occasional respiratory crepitations in bases, abdomen soft and non-tender.  I have arranged an USS bladder and kidneys to exclude any high residual volumes or obstructive neuropathy.  Thank you for your advice on any further management you would recommend for this patient.

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Current Medication; Aspirin, Daktocort, Movicol

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You’ve already answered – or are in the process of answering – the first question – does he have urinary retention and obstruction? He is of the right age and sex and is known to have prostatic disease. He is otherwise well, with no causative medicines and no hypertension to treat. As he is well, I’m guessing that he has‚ “gone off” and has now plateaued but it would be important to repeat all these to make sure this isn’t an acute renal failure that’s getting worse. If he demonstrates blood ++++ and/or protein ++++ we would be concerned.

Might I suggest that if his scan is normal, and especially if his U&E are getting worse, you ask us to see him? I’m hopeful however that this is good old obstruction which will improve with catheterisation. If his scan is positive, I’d have thought that the latter should be done without delay.


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Antihypertensives in Persistent Hypertension (7)

This 81 year old gentleman has raised BP, with systolic blood pressure varying between 170-200mmHg.  He has type 2 diabetes on insulin and regular diabetes OPD reviews.

Current medication; Atenolol (50mg OD), Furosemide, Simvastatin, Ferrous sulphate and allopurinol.

Amlodipine was previously stopped as it caused increasing ankle swelling.  He has also had a previous reaction to alpha blockers and ACE-I too. Candesartan has now been stopped.

He remains hypertensive and I am unsure how to proceed with regards to the medical management of this patient’s raised blood pressure, especially as his eGFR has recently decreased after titrating up his dose of Candesartan and remains so despite stopping it.

Could you please advise?

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Blood results;

2 Months ago – Urea 15.6 / Creatinine 135 / eGFR 44 / Sodium 144 / Potassium 4.2.

Today – Urea 21.4 / Creatinine 164 / eGFR 35 / Sodium 140 / Potassium 4.6.

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He is an elderly type II diabetic, very likely to have stiff and possibly calcified vasculature, which makes achieving good blood pressure control difficult.  He can’t take amlodipine (and almost undoubtedly other CCBs of the same class – eg. nifedipine), ACEIs and alpha blockers.  He is already on a decent dose of atenolol and furosemide.

I don’t think that trying other agents from same classes is likely to help. You could try and reintroduce the ARB when the eGFR is better and titrate up to find a small dose that doesn’t impair eGFR

Diltiazem and verapamil are too likely to cause bradycardia with the atenolol.

You can certainly try some of the centrally-acting agents like moxonidine or methyldopa but they often have more side-effects than the new classes of agent.

You should certainly encourage anything you can see regarding lifestyle changes – low salt intake, weight loss etc but at this age, I’m not sure I see a lot of leeway here either

Thereafter you may have to accept that blood pressure control is suboptimal and the risks that go with that.

Other comments:  There are patients in whom desirable BPs cannot be achieved without unacceptable side-effects, and you can discuss this with the patients. This is particularly common in elderly patients with stiff vasculature who often also develop severe postural symptoms with vasodilators. Clonidine is another centrally acting agent that could be tried and low dose spironolactone may be worth a try. It isn’t clear what happened with ACEs and ARBs. Might aliskiren be worth trying?


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Decreasing GFR in a Diabetic (6)

I would appreciate your advice about this 78 year old lady with IHD and NIDDM diagnosed 12 years ago. She was diagnosed with CKD stage 3 four years ago in 2006 (this is the first time her creatinine was elevated). Her renal function is steadily declining with a current eGFR of 32

PCR was 0.08 on 4/8/09 and an abdominal ultrasound scan showed normal kidneys in February 2006. Last HBA1c was 7.4 in July 09. BP is 138/78. She is almost stage 4 CKD

1) Should I refer her to a renal clinic?
2) Should I alter her medication (eg. Metformin)?
3) Do you have any other suggestions?

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Current Medications;

Aspirin 75mg OD, Simvastatin 10mg OD, Co-dydramol prn, Bumetamide 1mg OD, Allopurinol 300mg OD, Omeprazole 20mg OD, Amitriptyline 20mg nocte, Metformin 500mg TID, Lisinopril 10mg OD, Ferrous sulphate 200mg BD

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Her function is actually remarkably stable – losing 0.5mls/min/yr in terms of eGFR.

Her BP is close to adequate – target would be <130/80

She has no significant proteinuria on an ACEi.

She is appropriately on a statin, aspirin and ACEi.

The big issue is metformin. She is close to where Metformin should be stopped on the basis of absolute GFR, but she looks, on basis of all evidence, to be at low risk of progression in terms of renal disease. Stopping metformin will potentially de-stabilise her diabetic control and therefore a pragmatic approach would be to discuss the risk with her and leave her on Metformin.

However she should understand clearly that if she develops any intercurrent illness -especially vomiting or diarrhoea, she should stop both metformin and lisinopril until she has recovered.

I do not think there is any added value in her coming to a renal clinic.


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Proteinuria in Type 2 Diabetic (5)

This 63 year old gentleman is a type II diabetic with treated hypertension.  He attended for review 2 weeks ago and had an ACR sent as part of his diabetes care.  The urinary ACR was high with an albumin of 166, creatinine of 2.91 and ACR of 57.4.  The ACR was repeated with an MSU – the MSU was negative with no evidence of red cells.

When I saw the patient today I changed him on to gliclazide from pioglitazone, along with his metformin, and aim to titrate this up to try and get better diabetic control.  The patient is on an ACEi and his BP today was 132/78.

Looking back in the patient’s record he has had problems with right hydronephrosis, left sided renal calculi and a previous renogram showed some scarring. Since then he has had some episodes of renal colic and received lithotripsy in 20 years ago. He has not been troubled by renal colic recently.

My enquiry really is to get some advice as to whether an ACR at this level in this situation requires any further investigation or input from the renal service? Or should we continue to monitor and control his BP? Also at what level would you want to see someone with a high ACR?

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Medications;
Zopiclone, Quinine, Metformin, Sildenafil, Glicazide, Amlodipine, Fosinopril, Co-codamol, Bendroflumethiazide, Atorvastatin, Aspirin, Diclofenac

A summary of the results for this patient;

Urine 2 years ago – ACR 12.5 mg/mmol
Urine 2 weeks ago – ACR 57.3
Urine today – ACR 55.2

Blood Today – Urea 5.0 / Creatinine 72 / eGFR> 60 / Sodium 138 / Potassium 4.0 /  HBA1c  8.1

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Assuming there is no microscopic haematuria, then I think it is fair to assume that the raised ACR is due to diabetic nephropathy.  At that level, I would be looking to improve his BP further – ideally a target of 125/75 to be sure we match current recommendations.  The ACEi is indicated as he is a diabetic with proteinuria.  In some patients adding in an ARB may improve BP and reduce proteinuria further. (Controversial whether that improves outcomes though).

I would have some concerns about a diabetic patient (albeit good renal function) on the combination of an ACEi, Metformin and regular NSAIDs. Essentially he must discontinue the ACEi and NSAID in the event of any intercurrent illness such as diarrhoea, vomiting or fever. I would review whether he needs regular NSAID.


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Persistent Microscopic Haematuria (4)

An 81 year old lady has persistent microscopic haematuria and negative MSUs.  She is also on warfarin (last INR 3.4) for AF and has hypertension (last BP 162/80).

She has a history of cutaneous vasculitis and was seen by dermatology regarding a lesion on her leg a few years ago, but this all seemed to settle.  Urology investigated the same problem of microscopic haematuria 2 years ago and all investigations were normal.

Her ESR is slightly up at 28, but I wonder if the most likely cause is her raised BP and possibly warfarin use, but I would be grateful for your advice as to whether I should be doing anything else or you would wish to see her?

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Results of investigations are as follows;
Blood – ESR  28 / CRP – 2 / eGFR 51  (stable compared to previous results)

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Given your history and normal urological investigations, I would be tempted to just carry on doing what you’re doing, albeit with some further BP control.

It seems unlikely that after this long without progression, her haematuria is caused by systemic vasculitis, but an ANCA would be informative if positive.

However the golden rule is that with normal urological investigations, normal renal function (eGFR of 51 if stable will do at 81), no proteinuria and normotensive, then microscopic haematuria can simply be observed. I would monitor these variables – infrequently – and see what happens. We can always review the situation if things are changing but I think she’ll just remain stable.


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Hyperkalaemia in Polycystic Kidney Disease (3)

I was looking for a little advice regarding this 68 year old lady with polycystic kidney disease – either with regard to her medication or whether or not you felt she should be reviewed in clinic.

She had routine bloods and BP performed several weeks ago, her BP was 119/89 mmHg and her bloods came back with a raised ALP of 138 mmol/L, a potassium of 5.3 mmoml/L, an eGFR of 26 (previously 27) and her FBC was ok. These were repeated and her potassium remains elevated at 5.4 mmol/L, with a now normal ALP, calcium and phosphate. Her eGFR is now 23.

In view of her persistent hyperkalaemia and reduced eGFR I was wondering if she should reduce her lisinopril, this would obviously potentially increase her BP and reduce the nephroprotective effect. I have made no alterations at present and look forward to hearing your opinion. If you feel she requires a clinic review please let me know.

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The only other information available was her list of current medication; Lisinopril 10mg, Atenolol 50mg, Atorvastatin 20mg (not very compliant), Bendroflumathiazide 2.5mg OD, Quinine 300mg

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BP seems well controlled on current medications and I would be inclined to leave them unaltered; the potassium is ok.

Renal function is declining slowly – not out of keeping for ADPKD. I would recommend that she be referred back to clinic if the eGFR fell to less than 20.

Two things worth checking;

  1. Bicarbonate level – if she is becoming more acidotic it might explain the small rise in potassium
  2. PTH – rising PTH, in the context of secondary hyperparathyroidism, is a possibility to explain the rise in ALP. If PTH >180 then worth starting her on a small dose of oral alfacalcidol (0.25 mcg/day).


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Things to read:

  • Edinburgh Renal Unit – GP Referral criteria
  • Clinical Review of Hyperkalaemia in BMJ – Moffat J Nyirenda, Justin I Tang, Paul L Padfield, Jonathan R Seckl. Hyperkalaemia. BMJ 2009;339.
  • Edinburgh Renal Unit – Inherited Conditions