Renal Function Tests Clinical Cases PDF

Renal function tests Clinical Cases Dr Sheromna Sewpersad Department of Chemical Pathology University of Pretoria NHLS – Tshwane Academic Division Acute Kidney Injury AKI is characterized by rapid loss of kidney function, with retention of urea, creatinine, hydrogen ions an...

Renal function tests Clinical Cases Dr Sheromna Sewpersad Department of Chemical Pathology University of Pretoria NHLS – Tshwane Academic Division Acute Kidney Injury AKI is characterized by rapid loss of kidney function, with retention of urea, creatinine, hydrogen ions and other metabolic products and, usually but not always, oliguria AKI often develops in patients who already have CKD or are severely ill, with multiple organ involvement. AKI can be divided into three categories, according to whether renal functional impairment is related to: decrease in renal blood flow (pre-renal) intrinsic damage to the kidneys (intrinsic) urinary tract obstruction (post-renal) Pre-renal causes Decreased blood flow to the kidneys Dehydration Hypotension Haemorrhage Septicaemia Low cardiac output Burns Intrinsic renal Specific kidney diseases and systemic disease affecting kidneys, e.g. rapidly progressive glomerulonephritis systemic lupus erythematosus vasculitis Nephrotoxins non-steroidal anti-inflammatory drugs (NSAIDs) aminoglycosides x-ray contrast mediaa plant toxins some anticancer drugs Intrarenal obstruction, e.g. Bence Jones protein Post-renal Bilateral obstructing kidney stones Prostatic enlargement (benign or malignant) Other urinary tract neoplasms Retroperitoneal fibrosis involving both ureters Neurogenic bladder AKI - Biochemical findings Hyperkalaemia ↓ Bicarbonate Hyperphosphataemia Hypocalcaemia ↑ creatinine Hyponatraemia ↑ urea ↑ magnesium ↑ hydrogen ions ↑ urate Case 1 History A 25-year-old man sustained multiple injuries in a motorcycle accident. He received blood transfusions and underwent surgery. Examination Clinically dehydrated Blood pressure was 90/50 mmHg. The total urine volume passed during his first 24 h of admission was only 500 mL. Results Serum: Potassium 5.6 mmol/L Urea 21.0 mmol/L Creatinine 140 μmol/L eGFR 57 mL/min/1.73 m2 Osmolality 316 mmol/kg Urine: Sodium 5 mmol/L Osmolality 650 mmol/kg Results Serum: Potassium 5.6 mmol/L Summary Urea 21.0 mmol/L Serum urea is raised to a much greater Creatinine 140 μmol/L degree than creatinine. eGFR 57 mL/min/1.73 m2 The urine is concentrated but with low Osmolality 316 mmol/kg sodium. Urine: Sodium 5 mmol/L Osmolality 650 mmol/kg Results Serum: Potassium 5.6 mmol/L Urea 21.0 mmol/L Creatinine 140 μmol/L eGFR 57 mL/min/1.73 m2 Osmolality 316 mmol/kg Urine: Sodium 5 mmol/L Osmolality 650 mmol/kg Interpretation The results are consistent with pre-renal AKI. The urine contains little sodium and the urine osmolality is twice that of serum These are normal physiological responses, implying that intrinsic renal function is intact and that the ability of the kidneys to function normally is constrained only by hypoperfusion. Discussion The distinguishing features of pre-renal AKI as opposed to intrinsic kidney injury listed in the table above are not absolutely reliable. They are all invalidated if the patient has been given diuretics Osmolalities are invalidated by the use of x-ray contrast media. In practice, it is often not possible to distinguish between pre-renal and intrinsic renal injury using biochemical tests Also, if untreated, pre-renal AKI progresses to intrinsic renal injury. Concentrated, sodium-poor urine is a more reliable indicator of pre- renal AKI than a dilute sodium-containing urine is of intrinsic renal injury, because the latter is appropriate for a well-hydrated, healthy person. Oliguria is not a constant feature of AKI. Discussion The increase in serum urea concentration in this patient is greater than the increase in creatinine. The patient was given extra fluid intravenously and this resulted in a diuresis. The elicitation of this response may be the only way of distinguishing pre-renal from intrinsic kidney injury. eGFR may be misleading in this case Chronic Kidney disease Many disease processes can lead to progressive, irreversible impairment of kidney function. Glomerulonephritis, diabetes mellitus, hypertension, pyelonephritis, renovascular disease and polycystic kidneys account for the majority of cases where a cause can be determined. In effect, all these conditions lead to a decrease in the number of functioning nephrons CKD metabolic features Impairment of urinary concentration and dilution Impairment of electrolyte and hydrogen ion homoeostasis Retention of waste products of metabolism Decreased calcitriol synthesis Decreased erythropoietin synthesis Dyslipidaemia Reduced degradation of insulin and insulin resistance Other endocrine abnormalities  CKD Biochemical findings Hyperkalaemia ↓ eGFR ↓ calcitriol ↓ testosterone Hyperphosphataemia ↓ Bicarbonate ↓ oestrogen ↑ creatinine Hypocalcaemia ↓ renin ↑ urea Hyponatraemia Abnormalities of thyroid ↑ magnesium function tests ↑ hydrogen ions Abnormal glucose tolerance ↑ ALP ↑ insulin (caused by insulin resistance) Case 2 History A 56-year-old man presented to his family doctor with weight loss, generalized weakness and lethargy of 6 months’ duration. During this time, he had been passing more urine than usual, particularly at night. He had become impotent. Examination He looked anaemic and had a blood pressure of 180/112mmHg. His urine contained protein but no glucose. Results Sodium 130 mmol/L Potassium 5.2 mmol/L Bicarbonate 16 mmol/L Urea 43.0 mmol/L Creatinine 640 μmol/L eGFR 8 ml/min/1.73 m2 Calcium (adjusted) 1.92 mmol/L Phosphate 2.42 mmol/L Alkaline phosphatase 205 U/L Plasma: glucose (random) 6.4 mmol/L Haemoglobin 91 g/L Results Sodium 130 mmol/L Potassium 5.2 mmol/L Bicarbonate 16 mmol/L Summary Urea 43.0 mmol/L Very low eGFR, with low sodium, Creatinine 640 μmol/L calcium, bicarbonate and haemoglobin. eGFR 8 ml/min/1.73 m2 High phosphate. Normal glucose. Calcium (adjusted) 1.92 mmol/L Phosphate 2.42 mmol/L Alkaline phosphatase 205 U/L Plasma: glucose (random) 6.4 mmol/L Haemoglobin 91 g/L Discussion ? diabetes mellitus, but the absence of glycosuria made this unlikely The results are typical of CKD. Failure of the kidneys to concentrate urine adequately results in polyuria and nocturia. Oliguria is a late feature of CKD. The history suggests slowly progressive, rather than acute, kidney disease. The presence of anaemia and the raised alkaline phosphatase are consistent with the diagnosis, although they are not specific findings. CKD-MBD CKD-MBD – endocrine effects Inhibited calcitriol synthesis Decreased testosterone synthesis Decreased oestrogen synthesis Decreased renin synthesis Abnormalities of thyroid function tests Abnormal glucose tolerance with hyperinsulinaemia caused by insulin resistance Conclusion Biochemically there is a lot of overlap on the features of AKI and CKD, however, the history, length of symptoms as well as other endocrine markers will give an indication of the acute or chronic nature of the kidney injury It is important to screen for the start of kidney injury in at risk individuals in order to optimize all other factors to prevent accelerated progression of the injury Chronic kidney disease is not easy to treat, is rarely reversible and results in a multitude of other systemic dysfunction.