A patient with big kidneys

A 48 year old man is found to have BP 170/95 and a follow-up blood test shows eGFR 55.  The abdomen seems to contain hard masses.  On following this up, this investigation is undertaken:

PKD liver and kidney MRI radiopaedia 5202

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So that’s the diagnosis.  What is the prognosis likely to be?  Is there anything you can do to alter it?

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This is advanced PKD with very large kidneys and not much normal kidney tissue in between the cysts. This patient is likely to be heading for dialysis and/or a renal transplant. It is amazing that liver failure is extremely rare in PKD, despite sometimes massive cyst formation – though there can be physical symptoms from all this extra volume in the abdomen.

PKD accounts for close to 10% of end stage renal disease in most countries.

Management of PKD has been mostly symptomatic until recently, but the first drug to slow down the progressive growth of cysts is now licensed: Tolvaptan, an ADH receptor antagonist.  CKD issues in PKD are the same as for any other patient with renal impairment.

Further info

The image shown is courtesy of Prof Frank Gaillard (Radiopaedia)

A girl with facial swelling

[pic from Thyolo] A 14 yearl old schoolgirl is referred from Thyolo District Hospital, Malawi, complaining of facial swelling for 3 weeks, worse in the morning.  3 days later she developed bilateral leg swelling and increasing abdominal distension with some suprapubic colicky pains.  She reported concentrated urine but no haematuria.  There was no significant past medical history but 1-2 weeks previous to her symptoms she was treated for malaria when she had a fever.  Anaemia was noted at that time and she was given Albendazole and ferrous sulphate.  A week before admission she was treated for vaginal discharge with Gentamicin 240mg IM one dose, and a course of Doxycycline and Metronidazole.  She had also taken some herbal medicines for her symptoms.

She now complains of feeling ill, anorexia, and is vomiting once or twice a day.

Her father works on a tea estate as a labourer.  The family can afford 3 meals a day.

On examination she was unwell but not distressed, appeared well nourished.  Temperature 36.5C, pulse 96, BP 168/94, respiratory rate 16.  She had pale conjunctivae and facial oedema that she said was improved.  Pedal oedema had also mostly resolved.  There were no skin lesions or rash.  Throat was normal and she had no lymphadenopathy.  Her JVP was not elevated. Heart sounds were normal.  There was evidence of some ascites but again this seemed to be improved.

Urine dipstick showed blood 3+, protein 3+, and was negative for leucocytes and nitrite

Before showing results, what syndrome does she have?  What do you think the diagnosis is likely to be?

Case contributed by Emmanuel Mwabutwa

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  • HIV test negative
  • Pregnancy test negative
  • Hb 5.3 (MCV 70), wbc 4.3, plats 170
  • Creatinine was 19.3 mg/dl (1700 micromol/l) 3 days ago, having risen from 15.3 mg/dl (1350 micromol/l) 4 days previously.
  • Ultrasound showed kidneys to be normal in size but bright in echo pattern.  It confirmed ascites.  A cardiac echo showed a 1.6cm pericardial effusion but normal ejection fraction (76%) and appearances. The right atrium and hepatic veins were dilated.

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She has acute nephritic syndrome – fluid retention, hypertension (BP very high for a 14 year old) and renal impairment with strongly positive dipstick tests for haematuria and proteinuria.  These confirm glomerular disease.

The most likely diagnosis is classic post-infectious glomerulonephritis.  The normal kidney size and lack of left ventricular hypertrophy support an acute condition, rather than an exacerbation of something chronic.

She also has severe anaemia with microcytosis suggesting iron-deficiency.  Anaemia is frequent in the population and can be multifactorial related to malaria, diet, or other factors.

Her renal impairment is severe and life-threatening.  We do not have a potassium result.  Usually post-infectious glomerulonephritis in children resolves spontaneously, and there are probably many sub-clinical cases. At its most severe, dialysis may be required, but good recovery is still usual.  Even severe cases can usually be managed conservatively:

  • Diet:  Limit salt intake (about zero is right if they are oedematous and hypertensive); limit potassium intake
  • Restrict protein intake but provide plenty of calories.  Oedema can hide severe wasting
  • Loop diuretics relieve fluid retention in all but the most severe cases, and improvement in fluid balance improves blood pressure, though additional measures may be required.

Further info

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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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.

 

A call from the bone marrow transplant unit

They are concerned about the renal function of a 43yo lady who is day 26 post allogenic stem cell transplant for relapsed Acute Myeloid Leukaemia (conditioning with alemtuzumab, melphalan and fludarabine.  Her pre-transplant renal function was normal (creatinine around 60umol/L, eGFR>60ml/min), but has been on a pattern of fluctuating deterioration since around day 5 post transplant, reaching a level today of 415umol/L, eGFR 10ml/min, Urea 17.9, K+ 4.3, Na 143, HCO3 18).  Initial declines co-incided with episodes of sepsis and i.v Gentamicin use.  The patient has also been on Cyclosporin A microemulsion as prophylaxis against graft-versus-host disease, and has had a series of high serum trough levels (generally >300, target <200).  Cyclosporin has now been discontinued and replaced with Tacrolimus, with an initial trough of 15.1, and a Cyclosporin level which is still high at 220. Her weight is currently down 7kg from initial admission, and fluid balance demonstrates ongoing high (2-3L/day) urine output, with around 2L/day oral intake.

See more of the history or other available results?

Platelets have been consistently low (<20).
Blood film 2 days ago showed no evidence of red cell fragmentation.
Renal tract USS showed normal sized unobstructed kidneys.
Urine dipstick +haematuria, no proteinuria.
MSU – growing yeasts (further classification pending).

[/wptabs]

Now consider what advice you would give.

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Now read what the expert wrote

 The cause for this patient’s renal impairment is not certain, with a number of significant differentials

1)   Volume depletion.  Falling weight & high urine output would be consistent with this.  Impaired concentrating ability leading to a high obligate urine output can be a feature of both aminoglycoside toxicity and acute interstitial nephritis

2)   Urinary sepsis.  This will deliver an additional renal ‘hit’ and it is of note further treatment for a fungal urinary tract infection is needed.

3)   Acute Interstitial Nephritis.  The patient has been exposed to multiple courses of antibiotics over the preceding 4 weeks, which would be the most likely trigger & is also on a proton pump inhibitor.

4)   Aminoglycoside Toxicity.  Gentamicin was administered earlier in the clinical course- it seems unlikely this is the sole cause of the current problems but could then contribute to (1) and would be a sensitizing factor to other insults.

5)   Calcineurin Toxicity.  The patient currently has supra-therapeutic and potentially toxic levels of two calcineurin inhibitors at the same time, which have both haemodynamic and tubulotoxic effects on the kidney.

6)   Thrombotic Microangiopathy.  Chemotherapy, malignancy and CNIs are all associated with the development of a renal TMA.  This is associated with low platelets, although in this patients case the low platelets have persisted since her induction chemotherapy, and the absence of red cell fragments is strongly against this diagnosis (as is the lack of blood+protein in the urine dipstick)

Advice:  Efforts should be made to address all reversible factors in the above differential.  Ensure fluid replete and aim for net positive fluid balance over the coming weekend.  Treat sepsis.  From a renal perspective it would be advantageous to withhold Tacrolimus- but the risks of this precipitating GVHD need discussed with her consultant haemato-oncologist.  Suggest repeating blood film with particular attention to features of TMA and checking LDH (raised in intravascular haemolysis).  Check renal function on a daily basis and liase with the renal team.  If renal function continues to deteriorate patient will require transfer into the renal unit for consideration of renal replacement therapy and diagnostic biopsy (although this would be problematic given the current platelet count).

A call from the hepatology ward

A call from the Hepatology FY1:  She has been asked to ring due to concerns on the morning ward round about worsening renal function – specifically do we think this is hepato-renal syndrome?

56yo with history of alcohol excess, chronic obstructive airways disease and known cirrhosis with and previous oesophageal varices (in banding program).  Admitted 5 days previously with worsening jaundice and mild confusion.  An ascitic tap was performed on day 1 and a Bonano catheter inserted through which 4 litres of ascitic fluid was drained over the following 24 hours, with concurrent administration of 2x bottles of 20% human albumin solution.  Gram stain of the ascitic fluid demonstrated numerous neutrophil polymorphs, and the patient was therefore commenced on piperacillin/tazobactam at a dose of 4.5g tid i.v pending culture results.

Usual Medications:  Levofloxacin (stopped on commencing i.v. antibiotics),  Spironolactone (started in clinic, now withheld), Vitamin B co-strong, Seretide inhaler, Bisoprolol (now withheld), Citalopram.

Serial Blood tests                        Urea                        Creatinine

Clinic 2 months ago                         1.7                        53umol/L
Admission                                         5.5                        76umol/L
Day                                                    6.7                        89umol/L
Day 2                                                 7.1                        103umol/L
Day 3                                                 9.9                        131umol/L

What further information would you seek before giving your opinion?

See more of the history or other available results?

Other blood tests:, Bilirubin 121, Hb 121, WCC 13.2 (Neuts 11.1) Platelets 53, Prothrombin time 21 seconds

Abdominal USS :  shrunken nodular liver consistent with cirrhosis.  15cm Splenomegaly.  11cm kidneys bilaterally, no evidence of obstruction.

Blood pressure has been between 70 and 90mmHg systolic throughout the admission.   There has been a borderline temperature (max 37.8degrees). Urine output has not been completely documented due to poor patient compliance, however a urinary catheter has just been inserted.  Post catheter dipstick shows + haematuria, no proteinuria.

Now consider what advice you would give.

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Now read what the expert wrote

 This patient has significant acute renal dysfunction, on the background of chronic liver disease.  His normal sized kidneys and U&Es from clinic indicate that underlying renal function is normal and the dipstick result is against a primary parenchymal renal disease.

His hepatic impairment is a sensitizing factor for subsequent acute kidney injury.  The precise aetiology for the current dysfunction cannot be stated with certainty, but potentially includes components of

i)              Sepsis induced renal dysfunction (from presumed bacterial peritonitis)

ii)             Hypoperfusion from low BP (liver disease+ (i))

iii)           Over-diuresis & intra-vascular depletion from Spironolactone

iv)           Haemodynamic upset from large volume paracentesis (although replacement regime used was appropriate)

All the above lead to a state of pre-renal failure or established acute tubular injury.  An important differential would be the onset of the hepato-renal syndrome, characterised by oliguria in the face of volume repletion, extreme salt retention, progressive renal impairment, and a very poor prognosis (>90% mortality) in those not suitable for liver transplantation.

The common immediate management pathway for all of the above should be active volume resuscitation aiming to leave the patient intra-vascularly replete (this may be aided by the insertion of a central venous pressure line).  Investigation and treatment of sepsis should be undertaken, and consideration given to the use of laxatives to prevent constipation worsening encephalopathy.  Once the patient is volume replete (and assuming no diuretics are prescribed) then a spot urinary sodium can be measured, with a result <20umol/L  consistent with HRS.  The hepatologists may wish to consider the use of alpha-agonists such as midodrine as a means to support BP in the event of ongoing hypotension.  At this stage renal replacement is not required, however the renal team should stay involved with the patients care, as RRT could be required in the event of ongoing deterioration.   If this is occurring in the context of established HRS then careful discussion with the senior hepatologists would required as to the appropriateness of ongoing invasive and potentially injurious therapies in the setting of a very poor prognosis.

A call from the orthopaedic ward

A 68yo retired hospital cook had been admitted electively for total knee replacement 4 days previously. There was a background of longstanding rheumatoid arthritis, treated hypertension and CKD Stage 3 for which she no longer attends the renal clinic.

Serial Creatinines

Pre admission clinic               151umol/L

Day 1 post op                         176umol/L

Day 2 post op                          275umol/L

Day 3 post op                          329umol/L

Today (Day 4) post op             319umol/L

Renal dysfunction was first noted on Day 2 post operatively, and she has received a total of 7.5L i.v fluids since then.  A urinary catheter was inserted on Day 3, with hourly urine volumes initially 20-30mls/hr, but currently running at 50-100ml/hr.  Yesterday (Day 3) oxygen saturations were recorded at 87% and the patient placed on supplemental O2 which has raised the sats to 93-95%.  The FY1 states that there are crackles audible bi-basally on auscultation of the chest, but little evidence of dependent oedema.  The surgical registrar felt that the JVP was elevated and favoured administering IV furosemide.

The specific question posed by the senior surgical team is whether there is a role for the administration of i.v furosemide in this patient’s case given her reduced oxygen saturations and cumulative positive fluid balance, and what additional measures should be undertaken to ensure recovery of renal function.

What other tests might you request in this patient.  Is there anything else you would like to know about the patient’s management?  How would you answer their question regarding furosemide?

What further information would you seek before giving your opinion?

See more of the history or other available results?

Medications:  Bendroflumethiazide 2.5mg , Hydroxychloroquine, Losartan 50mg, Paracetamol 1g qds, Tramadol 50mg qds, Morphine 5-10mg prn.  (Losartan was administered up to and including post-op Day 2).

Chest X-ray : pleural thickening R base (present in 2010), prominent hilar vessels.

Renal tract USS : Kidneys Left 9.5cm Right 9cm, no evidence of obstruction, catheter seen in bladder.

Now consider what advice you would give.

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Now read what the expert wrote

On further questioning, it emerged that there had been relative hypotension (systolics 80-100mmHg) persisting from at least the immediate post-operative period to around Day 3.  For much of this time anti-hypertensives had continued to be administered, including the Angiotensin II receptor antagonist Losartan.  Hence the combination of pre-existing CKD, surgery, low BP (particularly in a patient with background hypertension and Losartan administration would offer a multifactorial set of renal insults to account for her acute on chronic renal failure.

Importantly, BP was now better, the potential nephrotoxic drug had been stopped, and urine output had risen with serum creatinine stabilized/fallen marginally over the last 24 hours.  With this combination (and a safe K+) there was no indication for renal replacement, and indeed if further insults could be avoided she was very likely to continue to recover.

Whilst my instinct over the phone was not therefore to administer furosemide, (and given in the surgical wards there are not middle grade physicians in routine attendence) I offered to review the patients fluid status myself.

Meeting the patient, she was lying flat in bed on 2L/min supplemental oxygen, had a respiratory rate of 10/minute and had difficulty staying awake whilst being examined.  Pupils were constricted.  T37.6.  BP 110/80.  HR 80.  Sats 94% on oxygen.  Dry crackles were present in both bases, more marked on the right side.  JVP was +3cm.  Sputum pot contained thick green sputum.

My impression/advice was therefore:

i)              Likely hospital acquired chest sepsis.  Start HAP antibiotics

ii)             Opiate toxicity due to declining renal function and drug accumulation.  Stop tramadol & morphine.  If strong opiate required consider fentanyl/alfentanyl due to safer pharmacokinetics in renal impairment

iii)           Low oxygen sats reflect (i) and (ii) rather than pulmonary oedema.  No indication for diuretics at present- fluid status appears appropriate.  Bibasal chest signs could represent atelectasis, but possibility of rheumatoid lung disease should also be considered.

iv)           Withold losartan at present.  There is no contraindication to re-introduction when renal function is normalised, but this would be best done after discharge with monitoring in primary care.

A 16 year old girl with oedema

A 16 year old girl presents to Queen Elizabeth Hospital, Blantyre with a two-month history of facial oedema.  It is worse in the morning, slightly better at night and not associated with shortness of breath or cough.  She has been well recently, with no intercurrent illnesses. Some kind of antimicrobial was prescribed a month ago, but the swelling was present then and has increased since.

On examination she is slim but has marked bilateral pitting pedal oedema and facial puffiness; her abdomen is also distended, with shifting dullness.  She is apyrexial.  General examination is unremarkable.  Her BP is 112/65, pulse 72.  She has reduced breath sounds and dullness to percussion at both lung bases.  Heart sounds and abdomen are normal and she has no neurological deficit.

A urine dipstick shows 4+ protein.  She has a serum creatinine of 60 micromol/l (0.7 mg/dl) and a normal blood count.  Tests of liver function, serum proteins are not available.

  1. What is the differential diagnosis?
  2. Renal biopsy is not immediately available here.  What management will you recommend?  How will you advise her and her parents?

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With 4+ proteinuria and oedema there can be little doubt that she has nephrotic syndrome.  It is ‘pure’ nephrotic syndrome, meaning heavy proteinuria without any haematuria, which puts it at the extreme left hand end of the spectrum (see Glomerulonephritis) and makes it significantly less likely that it is caused by post-streptococcal glomerulonephritis or other disorder more toward the ‘nephritic’ end of the spectrum.

She should severely restrict salt intake: oedema is caused by salt retention.  Diuretics are often required, usually loop diuretics.

HIV is an important condition in this region.  An HIV test is important both because the condition could be a manifestion of HIV affecting the kidney, and because most active treatments for nephrotic syndrome involve immunosuppressive agents.

Minimal change disease would be the most likely explanation in a Caucasian girl.  However FSGS is more common as a cause of nephrotic syndrome in Africans: one of these two conditions is most likely. SLE is very unusual before menarche.

If she is HIV negative, a trial of prednisolone, 1mg/kg/day for a few weeks would be worthwhile.

Further info

This case is was contributed by Fran Th’ng and Gavin Dreyer

A 25 year old woman with a rash and raised creatinine

A 25 year old woman is referred with a 6 month history of fatigue, joint pain, pleuritic chest pain and facial rash. Three months ago at another hospital she was found to be unwell with a Creatinine of 500 micromol/l, Hb 8.2 g/dl, and urinalysis showed 3+ protein, 3+ blood. She was treated with some tablets (identity unknown) and a subsequent creatinine was 200 and Hb rose to 12 g/dl. Now she is unwell again.

On examination she has a rash around her nose and on her cheeks. She is febrile, 38.2C, and has mild swelling of her left and right MCPJ. She is slim and does not look Cushingoid. BP 155/87. There is no oedema and examination of chest, cardiovascular system and abdomen are normal. She has a platelet count of 50 and Hb 6.2g/dl, Creatinine 430 micromol/l, and urinalysis continues to show 3+ for both protein and blood.

Three questions:

  1. What is the likely underlying diagnosis?
  2. What other urgent (not too complicated) test results are important?
  3. How would you treat the underlying disease given that a renal  biopsy is not possible?

Thanks to Dr Gavin Dreyer for this case.

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Diagnosis:  Lupus seems the most likely underlying diagnosis.

Tests (1) She had a high level of Malaria falciparum parasitaemia. (2) She was HIV non-reactive.
Neither infection would do well with immunosuppressive therapy for lupus. The level of HIV positivity in the region is high, but in sick patients, in particular medical inpatients, it is much higher (up to 80%).
Ideal initial treatment according to WHO should be Artemisinin combination therapy, but it is not generally affordable so Quinine is still most commonly used. She responded to treatment and her Hb rose.

Treatment beyond this point is difficult, but almost certainly she has aggressive inflammatory disease in view of the creatinine changes, and will need cyclophosphamide. Some might argue for MMF in a young woman, but it is less well tested, and much more expensive.

Other diagnostic possibilities?
Classic HIV nephropathy usually has a more extreme nephrotic phase. Of course many other renal pathologies can occur in HIV infection.

Further info

An HIV positive woman with low eGFR

A 38 year old woman who has been on anti-retroviral therapy for 3 years is found to have a creatinine of 230 micromol/l (2.6 mg/dl).  She is taking Tenofivir, Efavirenz and cotrimoxazole and has been compliant with therapy.  She complains of recurrent dysuria and frequency, as well as intermittent fevers which do not always seem related to urinary symptoms.  She describes some vaginal discharge.

On examination she is thin but not emaciated.  She has no oedema.  Her pulse is 64, blood pressure 110/60, chest is clear, cardiovascular system normal.  She has mild non-specific abdominal tenderness but no masses.

Urine dipstick is positive for nitrites and leucocytes, blood 1+.

What type of disease process do you suspect?  What further features or investigations would you immediately seek?

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She has marked renal impairment; that creatinine corresponds to an eGFR of about 26.  She already has possible explanations for renal disease from her diagnosis of HIV and the fact that she is on anti-HIV drugs, many of which have renal side effects, including crystallization, interstitial nephritis, tubular injury.

A key observation is the bland urinary sediment, showing little protein or blood, which essentially rules out severe glomerular pathology.  HIV nephropathy is a glomerulopathy, so it is an unlikely explanation. Using the pre-renal/renal/post-renal algorithm, this makes you home in on

  • Pre-renal causes.  She doesn’t sound very dehydrated, but pre-renal causes include arterial and small vessel disease; for instance thrombotic microangiopathy can occur in HIV.
  • Interstitial or tubular causes (drugs particularly likely to be implicated; tenofivir is associated with tubular injury)
  • Obstruction

The key investigation in any patient with renal failure and urinary symptoms is renal imaging.  Ultrasound is quick, non-invasive, risk-free, and almost always first choice; it should be part of the investigation of almost any patient with unexplained new severe CKD.  It showed bilateral hydroureter and hydronephrosis without distention of the bladder.

Hope you had also written that vaginal examination is one of the things that you must do here.  She had advanced cervical cancer involving both ureters.

She also had a CD4 count of 93 despite her anti-HIV therapy, with PCR showing 5,000 copies per ml, suggesting anti-retroviral failure.  In a well-resourced setting you would consider testing for drug resistance.

Further info

Thanks to Fran Th’ng and Gavin Dreyer for this case.

Renal failure from the HIV clinic

A 32 year old man presents wtih 3 days of vomiting, nausea, and malaise.  HIV was diagnosed 6 months ago but he has not been started on ant-retroviral therapy.  He has no other significant past medical history.

He is apyrexial.  BP is 100/60 and pulse 82.  He has no oedema.  JVP is not visible when lying flat.

Urine dipstick shows 1+ protein only.  The only other investigation available is serum creatinine – 700 micromol/l (8 mg/dl).

What do you think are the main diagnostic possibilities here?  What additional key questions would you like to ask? What would your initial management be?

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(To follow!)

Case contributed by Fran Th’Ng and Gavin Dreyer