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Last updated: Acute Kidney Injury…
on 10 Apr 2017

November 2013

The 'Cardio-Renal' Syndrome

Shams-Ulisham Ilyas MBChB, Timothy Evans MRCS and Yogita Aggarwal MRCP 

Introduction

We present a case of gross fluid overload and stage 3 acute kidney injury secondary to severe cardiac failure.  No underlying renal aetiology was demonstrated.

Background

A 60-year old female patient was admitted feeling unwell for 3 weeks with symptoms of worsening exertional dyspnoea and a marked reduction in exercise tolerance from 50 yards to 5 yards over the last one month. Particular symptoms included

  • Worsening orthopnoea requiring 3 pillows to aid sleep.
  • Worsening long standing peripheral oedema, with the rapid upwards spread of oedema from her lower legs to her thighs over the last 48 hours, and   
  • New onset nausea with frequent episodes of retching. 

She had seen her GP who suspected a lower respiratory tract infection and commenced a course of oral amoxicillin, which had not altered her symptoms. Her past medical history included:

  • Non-proteinuric Chronic Kidney Disease (CKD) Stage 3[i] with a stable creatinine of 80-90mmol/L (eGFR of 50-55ml/min/m3) since 1993
  • Chronic Persistent Atrial Fibrillation (AF)
  • Metallic mitral valve replacement (MVR) in 1998 for which she was on warfarin.
  • Endocarditis (no organism grown) in May 2013.
  • Type 2 diabetes mellitus (DM) with a HBA1c 43 (normal range) and no end organ involvement.
  • Predictable and infrequent exertional angina.
  • Hypertension with average readings of 148-160mmHg systolic and 85-90mmHg diastolic.

Medications included:

  1. Warfarin
  2. Ramipril
  3. Bisoprolol
  4. Lansoprazole
  5. Gliclazide
  6. Furosemide
  7. Simvastatin
  8. GTN spray

On examination the patient was unwell with clear evidence of fluid overload. Summary of findings included in table 1.

Investigations:  The admission blood and urine results were as follows, see Tables 2 and 3.

Initial Diagnosis:  Stage 3 Acute kidney injury secondary to gross fluid overload and renal congestion. 

Management: 

There were three prongs to this patient’s management.

1. Diuresis 

  • Daily weights 
  • Low salt diet            
  • Diuretics (IV furosemide over oral, due to poor oral absorption given gastric oedema in fluid overload. Combined loop   and thiazide diuretics to promote diuresis)
  • Daily UEs      
  • Fluid restriction 1L/day
  • Aim weight loss of 1kg per day

 

2. AKI screen 

Urine dip showed 2+ blood and following were requested:

  • C3/C4, ANA, ENA, ESR, ANCA – looking for a vasculitic process
  • CK  - to rule out rhabdomyolysis
  • MSU  and urine cytology - looking for infection and abnormal pathognomonic cells
  • Blood cultures - precautionary given the patient’s previous history of endocarditis. Blood and protein on urine dipstix analysis may suggest a post-infectious GN. Clinically the patient did not evidence for acute infection.
  • Serum and urine paraproteins screen: Although the urine alb:creat ratio (ACR) took a few days to process, despite the absence of protein on urine dipstix, a myeloma screen was requested as urine paraproteins are not detected on standard urine dipsticks. Myeloma can cause AKI but often in combination with a normocytic anaemia and hypercalcaemia.

(* All the above tests were normal.*)

3. Cardiac Evaluation

  • Echo evaluation of cardiac and valve function 

 

Clinical Progress:

With diuresis the patient’s kidney function slowly improve to a baseline creatinine of 88mmol/L, and her weight fell by 8 kg.   The diuresis occurred over a 2 week period.

Transthoracic Echo (TTE) evaluation confirmed an unstable prosthetic valve (MnPG 7mmHg), severe MR, moderate TR, severe pulmonary hypertension (estimated PASP 89 - 94mmHg), and mild RV dilatation with impaired systolic function.  The left ventricle LV was normal sized with good overall LV systolic function.  Bi-atrial dilatation was also noted.

After the TTE was done, th Cardiology team immediately transferred the patient to CCU and she was worked up for   to a combined mitral and tricuspid valve replacement surgery.

The patient successfully underwent the operation, with her creatinine returning to 82mmol/L when she was seen in renal clinic 3 months later.  She also had no evidence of decompensated fluid overload.

 

Learning Points:

In the presence of significant AKI, other non-renal causes of fluid overload should be considered, especially in the absence of nephrotic syndrome.

The patient’s AKI was due to combination of poor cardiac output and venous congestion. On improvement of the cardiac function with diuresis and then subsequent valve replacement, the renal function also returned to baseline.

References

Mullens W, Abrahams Z, Francis GS, et al.  Importance of venous congestion for worsening of renal function in advanced decompensated heart failure.  J Am Coll Cardiol. 2009 Feb 17;53(7):589-96.

Damman K, Navis G, Smilde T, et al.  Decreased cardiac output, venous congestion and the association with renal impairment in patients with cardiac dysfunction.  Eur J Heart Fail (2007) 9 (9): 872-878. 

 



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