A fifty year old gentleman, a known diabetic and hypertensive presented with exertional dyspnea and fluid overload. He was detected to have renal failure and associated evidence of cardiac disease, cardiorenal syndrome Type 4. He improved with decongestive therapy and conservative management. In view of the presence of microvascular complications of diabetes, he was diagnosed as diabetic nephropathy stage 5 and initiated on maintenance haemodialysis. The approach to diabetics with renal involvement and the issues in their management is discussed.
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Case summary
A fifty year old gentleman a known diabetic and hypertensive for eight years presented with exertional dyspnea of one month duration. Dyspnoea on exertion had been progressively worsening for one month with orthopnea for one day. He complained of cough accompanied with ½ a cup per day of mucoid non foul smelling, non blood stained sputum for last one month. He complained of swelling feet with worsening of dyspnoea for last four days. No h/o chest pain, PND, syncope, wheeze or fever. He was a chronic smoker (25 pack yrs) and a reformed alcohol consumer – 240 gms/day for 15yrs.
What would be your analysis of symptoms?
The exertional dyspnea is suggestive of cardiovascular system involvement. In a diabetic, hypertensive and chronic smoker, coronary artery disease or hypertensive heart disease would be common possibilities. Cough with wheeze in a smoker could be COPD in exacerbation with cor pulmonale accounting for the exertional dyspnea and swelling feet, however orthopnea, a sign of left sided cardiac involvement would be uncommon. Additionally, the duration of cough is too short to qualify for COPD. Infective causes of cough like tuberculosis need to be excluded although they cannot account for all symptoms.
He also complained of decreased urine output and puffiness of face for last four days. There is no history of altered behaviour, haematuria, smoky urine, nocturia, dysuria, hesitancy or precipitancy. Two years ago patient during evaluation prior to surgery for prolapsed disc was found a creatinine of 1.5mg%.
Does the differential diagnosis change in the light of the additional information?
The complaints of oliguria and puffiness of face suggests renal failure with fluid overload state. It is common for Type 2 diabetics, especially with accompanying hypertension to present with early renal involvement. Therefore, although the duration of diabetes is only eight years, the cause of renal failure could still be diabetic nephropathy. The presence of renal involvement two years ago is a clue to the chronic nature of renal involvement. An acute on chronic renal failure due to respiratory tract infection could account for the sudden worsening over one month.
On examination, pulse – 84 / min, regular, BP 190/110 mm Hg, respiratory rate 28/min, thoraco – abdominal , JVP – 8 cm above sternal angle, Facial puffiness, pallor and pitting edema in upper and lower limbs noted. Trophic skin changes in lower limb were present. No asterixis, Icterus, clubbing, cyanosis or lymphadenopathy seen. Respiratory system examination revealed extensive wheeze and coarse crackles. The heart sounds were normal with no pericardial rub. Liver was enlarged, span 15cm,soft, nontender and ascites was not elicitable. Fundoscopy revealed early nonproliferative diabetic retinopathy. Rest of neurological examination was normal.
What is your analysis with the given clinical findings?
The patient has anasarca with pallor and hypertension. The presence of diabetic retinopathy also suggests microvascular complications have set in. Diabetic nephropathy with fluid overload state can explain most of the signs and symptoms. An associated cardiac disease like coronary artery disease may be present. Diastolic heart failure is common accompaniment that may be contributing the signs of right heart failure. Cardiac asthma can account for the new onset wheeze in a diabetic. Diabetic nephropathy with a possible cardiac pathology, cardiorenal syndrome is the most likely diagnosis.
What is cardiorenal syndrome?
Cardiorenal syndrome (CRS) is a pathophysiologic entity involving the heart and kidneys where acute or chronic dysfunction of one organ may result in acute or chronic dysfunction of the other. CRS Type 1 reflects an abrupt worsening of cardiac function as is seen in acute cardiogenic shock or in a patient of congestive heart failure who has decompensated leading to acute kidney injury. CRS Type 2 comprises the group of patient with chronic congestive heart failure resulting in progressive chronic renal failure. CRS Type 3 consists of an abrupt worsening of kidney function (e.g., acute renal failure or glomerulonephritis) causing acute cardiac dysfunction (e.g., arrhythmia, ischemia, heart failure). CRS Type 4 refers to a state of chronic kidney disease (e.g., chronic interstitial nephritis, chronic glomerulonephritis) contributing to left ventricular hypertrophy and poor cardiac function. CRS Type 5 reflects a systemic condition like sepsis resulting in simultaneous cardiac and renal dysfunction.
Our patient seems to have Cardiorenal syndrome Type 4. The biochemical parameters, ECG and echocardiography will be needed to make a firm diagnosis.
Investigations revealed Hb 10.5g/dl, TLC 13300/cumm, DLC P91L7, platelets 2.78lac/cumm, Urine albumin 4+, granular casts+, blood urea 89mg/dL, serum creatinine 5.8mg/dL, serum Na 115mmol/L, serum K 3.1mmol/L, blood sugar fasting 102mg/dL, postprandial 156mg/dL,HbA1C 6.6%, serum bilirubin 0.5mg/dL, calcium 8.4mg/dL, phosphate 3.2mg/dL, iPTH 6.9pg/ml, CKMB 19mg/dL, serum iron 48 µg /dL, serum TIBC 243µg/dL, transferrin saturation 19.7%, HBsAg negative, Anti HCV Negative, HIV Negative. Ultrasound revealed medical renal Disease with bilateral renal cysts, size of right kidney 8.5 cms left kidney 9.5 cms. Chest radiograph showed cardiomegaly with prominent hilar markings. ECG showed T wave inversion in I, aVL,V4- V6 suggestive of strain pattern and left ventricular hypertrophy by voltage criteria. 2-D ECHO showed concentric LVH, No RWMA, EF 0.65,diastolic dysfunction, trivial TR and no AS/AR.
Could this patient have nondiabetic renal disease? Is there an indication for kidney biopsy to confirm renal diagnosis in this patient?
In a diabetic with kidney disease, it would be presumed that the proteinuria and azotemia is due to diabetic nephropathy especially if there is associated retinopathy and normal sized kidneys. There is no necessity to perform a kidney biopsy to confirm diabetic nephropathy as it would make no difference in the management. However, a diabetic is also prone to other nondiabetic renal diseases as in the general population that may need histopathological examination and warrant specific therapy. The clues that the renal failure is due to nondiabetic renal disease requiring a biopsy are summarised. Asymmetric kidneys or small sized kidneys are also clues to a nondiabetic renal disease but donot warrant biopsy. Our patient has near normal sized kidneys (right kidney small) with proteinuria and nonproliferative retinopathy, hence there is no requirement to biopsy. Retinopathy is present in 65% of cases of DMType2 with nephropathy, hence absence of retinopathy doesnot rule out nephropathy.
Biopsy not indicated when
Typical evolution of renal disease Concomitant retinopathy
Biopsy should be considered when
Renal manifestations are seen atypically (<10 years) early*
Dysmorphic erythrocytes/casts are found (nephritic sediment) in type 1 diabetes
Rapid deterioration of renal function of unknown cause is noted
Elevated serum creatinine without urine abnormalities
Heavy proteinuria (>5-8 g/day) persists despite lowering of blood pressure
* Only for Type 1 diabetes
What are the stages of diabetic nephropathy? What stage is the patient in?
The stages of diabetic nephropathy are as summarised in the table. Microalbuminuria is the earliest clinically detectable evidence of onset of nephropathy in a diabetic. About 20-25% of diabetics develop nephropathy in their lifetimes. The time after diagnosis has been validated after followup of Type1 diabetics and doesnot hold true for type 2 diabetics because the the time of onset of diabetes is not clearcut ina given case. It is not uncommon for clinically evident nephropathy to be present when type 2 diabetes is detected. Our patient has established renal failure, hence is in stage 5 diabetic nephropathy.
Stage
Glomerular filtration
Albuminuria
Blood pressure
Time interval
1 Renal hyperfunction
Elevated
Absent
Normal
At diagnosis
2 Clinical latency
High normal
Absent
3Microalbuminuria
Within the normal range
20-200 μg/min (30-300 mg/day)
Rising within or above the normal range
5-15 years
4 Proteinuria (overt nephropathy)
Decreasing
200 μg/min (300 mg/day)
Increased
10-15 years
5 Renal failure
Diminished
Massive
Increased
15-30 years
What is the difference in nephropathy in Type 1 diabetes and type2 diabetes?
Type 1 Diabetes with nephropathy
Type 2 Diabetes with nephropathy
Follows classical stages
Hypertension is usually due to renoparenchymal aetiology
Retinopathy 90-100 % concordance
Non diabetic renal disease rare
Less consistent
Primary hypertension commoner (metabolic syndrome)
Retinopathy 60% concordance
Non diabetic renal disease 20-30%
Define microalbuminuria. What is the relevance of finding microalbuminuria in a diabetic?
Microabuminuria is defined as the presence of 30-300 mg albumin/24 hrs urine collection or 20-200microgm/mt in a timed urine sample in atleast 2/3 samples over 6 months in the absence of fever, infection, physical exercise, uncontrolled blood pressure or sugar, cardiac failure or haematuria. The importance of the finding is that it indicates endothelial dysfunction and is a predictor of diabetic nephropathy in 80% and 40% Type1 and Type2 diabetics. It is also is a predictor of cardiovascular mortality and is strongly associated with insulin resistance and hypertension. In a given patient it is a clue to the clinician to institute aggressive control of blood pressure and hyperglycemia to prevent progression of diabetic nephropathy.
The patient was managed with loop diuretics, plain insulin, inhaled bronchodilators, nitroglycerine drip and oxygen therapy. After initial stabilisation, he continued to have raised serum creatinine, hence was initiated on maintenance haemodialysis as a case of diabetic nephropathy with ESRD.
What happens to the hyperglycemia with the onset of diabetic nephropathy? What treatment modifications are required to be made for glycemic control?
With the onset of nephropathy, the insulin requirement decreases and patient becomes more prone to hypoglycaemia because the half life of insulin is prolonged, renal gluconeogenesis decreases, food intake is decreased, half life of oral hypoglycemics is prolonged, diabetic gastropathy delays gastric emptying and patient frequently vomits food due to uraemia. Infact if a well controlled diabetic develops episodes of unexplained hypoglycaemia, then one needs to look for evidence of nephropathy. Biguanides and long acting sulfonylureas are contraindicated in the presence of renal failure. Glimepride and glipizide may be used if serum creatinine is less than 2mg/dL. With more advanced renal failure, patient should be shifted to insulin therapy.
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What are the measures that can prevent the progression of diabetic nephropathy?
Large randomised control trials like IDNT and RENAAL have provided clear evidence that angiotensin receptor blockers help to prevent progression of diabetic nephropathy. The ADVANCE trial provided similar evidence for angiotensin converting enzyme inhibitors. A target blood pressure of 130/80 mmof Hg is recommended for diabetics with proteinuria. Intensive treatment of hyperglycemia with tight blood sugar control has shown to reduce the incidence of micovascular complications including nephropatrhy in multiple studies like DCCT, UKPDS and ADVANCE. Cessation of smoking, avoidance of high protein diet and control of hyperlipidemia also seem to be beneficial. Once overt renal failure has set in then tight blood sugar control may not prevent further progression of nephropathy and the risk of hypoglycaemia increases, hence the physician should use discretion in prescribing antidiabetic therapy.
What are the issues in dialysis of patients with diabetic nephropathy?
Although diabetics with ESRD are candidates for all renal replacement therapy (RRT) options as nondiabetics, there are many factors that make it challenging to provide RRT in a diabetic. Associated coronary artery disease and diastolic dysfunction, high incidence of fistula failure due to atherosclerosed vessels, heparin (given during haemodialysis) related bleed due to associated retinopathy, decreased osmotic gradient and poor clearance in CAPD, poor tolerance to uraemic symptoms, diabetic cystopathy and gastroparesis, preponderance to low turnover bone disease, higher incidence of infections, autonomic neuropathy, elderly age group of patients with attendant social and logistic issues all contribute to poor survival in diabetics compared to nondiabetics.
Final diagnosis – Diabetic nephropathy in end stage renal disease with Cardiorenal syndrome Type 4
Commentary
Diabetic nephropathy has become the commonest cause of chronic kidney disease in both the western world and developing countries. Classical stages of diabetic nephropathy described in Type 1 diabetics may not be evident in the progression of kidney disease associated with Type 2 diabetics. Measures to prevent progression of diabetic nephropathy should be aggressively instituted. Patients of diabetes Type2 with kidney disease additionally have associated cardiac disease making the management of such patients challenging. Cardiorenal syndromes encountered in various situations have been recently described that have improved our understanding of the complex pathophysiology and may open new avenues of treatment in the future.
Take home message
- Diabetic nephropathy is the commonest cause of ESRD and developing countries are likely to face an epidemic in the next two decades.
- Cardiorenal syndrome (Types1-5) is a recently described pathophysiological condition that has furthered our understanding of the complex interrelation between heart failure and kidney failure in diverse clinical settings.
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