Teaching Case

A 44-year-old woman was admitted with a two-week history of breathing difficulty, abdominal pain and vomiting. On examination she had generalized anasarca. Laboratory assessments revealed: calcium = 2.3 mmol/L, creatinine = 680 mm/l, eGFR = 8.4 ml/min and urine protein/creatinine ratio = 140.1.

Axial CT of the abdomen shows the hyperdense bilateral normal sized kidneys (Fig. 1 e-i). Coronal and sagittal images show the same (Fig. 2). The hyperdensity is diffuse and spares the medullary region. CT also shows severe bilateral pleural effusions (Fig. 1 a, b) and moderate ascites (Fig. 1 c, d). Generalised anasarca was also noted in the form of subcutaneous oedema.

Renal calcification can be broadly classified into two groups: nephrolithiasis when the calculus is located in the collecting system; nephrocalcinosis when the calcification is in the renal parenchyma. Nephrocalcinosis can be subdivided into a medullary and a cortical form [2]. The most frequent causes are chronic glomerulonephritis and acute cortical necrosis. The aetiology of cortical nephrocalcinosis in this patient was the presence of chronic glomerulonephritis. Both ultrasound and CT can detect nephrocalcinosis earlier than plain abdominal X‐ray. Ultrasound demonstrates an increased echogenicity of the renal cortex, sometimes with acoustic shadowing. CT will display punctate band or tram‐line calcification in the basal and septal cortex with sparing of the medulla. In general, three different patterns are described in cortical nephrocalcinosis. Most commonly, a thin peripheral band of calcifications, often with extension into the septal cortex [2]. Two thin parallel calcified tracks (so called ‘tram‐line’) represent a second type of cortical nephrocalcinosis. The least common form consists of multiple punctate calcifications with a random distribution in the renal cortex. Other causes of cortical nephrocalcinosis include acute renal cortical necrosis caused by sepsis, toxaemia of pregnancy, drugs, snake bite, arsenic poisoning, extracorporeal shock wave lithotripsy, haemolytic uraemic syndrome, primary and secondary oxalosis, intrarenal infections in HIV‐seropositive patients (Mycobacterium avium, Pneumocystis carinii), amphotericin B, chronic pyelonephritis, acute and chronic renal allograft rejection, autosomal recessive polycystic disease and benign nodular cortical nephrocalcinosis [2].
Hyperoxaluria is a rare metabolic disorder of oxalate metabolism with excess production and/or excretion of oxalic acid in urine [1]. The excess oxalate is excreted through the kidneys, and the tubules of the kidneys are progressively but definitively damaged.
Cortical hyperdensity can be seen in unenhanced study as a result of cortical nephrocalcinosis. This differential should be borne in mind while evaluating cortical and medullary nephrocalcinosis in children [1].