Renal amyloidosis

Renal amyloidosis typically presents with nephrotic syndrome and accounts for a significant proportion of all nephrotic presentations in the elderly.

Renal involvement in systemic lupus erythematosus

Systemic lupus erythematosus can affect the kidney in a number of different ways. Typical patterns of renal involvement include focal or diffuse proliferative, membranous, mesangiocapillary (membranoproliferative) and crescentic glomerulonephritides. Interstitial damage, tubular defects and ultimately glomerular fibrosis and sclerosis can also occur.

Reference:

• Renal involvement in systemic lupus erythematosus. A study of 180 patients from a single center.

Drug-induced acute interstitial nephritis

The drugs that most commonly cause acute interstitial nephritis are penicillins, non-steroidal anti-inflammatory drugs and thiazide diuretics.

When the circulation is compromised, non-steroidal anti-inflammatory agents, angiotensin converting enzyme inhibitors (such as enalapril) and angiotensin-II receptor antagonists (such as candesartan) can have adverse haemodynamic effects on the kidney leading to a reduction in GFR, but ACE inhibitors and AT2 blockers are not associated with interstitial nephritis.

Hepatorenal syndrome (HRS)

HRS is defined as an acute, functional and progressive reduction in renal blood flow and glomerular filtration rate (GFR) secondary to intense renal cortical vasoconstriction in the setting of decompensated liver disease. Other aetiologies for renal failure in liver disease must be excluded. HRS can be classified as type 1, with a rapidly progressive decline in GFR (<2 weeks), or type 2, which is not as rapidly progressive (>2 weeks). Although not diagnostic, a low spot urinary sodium (<5 mmol/L) is in keeping with a diagnosis of hepatorenal syndrome (HRS), assuming that the patient does not have intravascular volume depletion.

Renal vein thrombosis

Nephrotic syndrome predisposes to renal vein thrombosis, which typically presents with flank pain, haematuria and a rise in creatinine.

Renal Disease and Pregnancy

Pregnancy in patients with significant renal impairment is associated with increased maternal and fetal complications. With this degree of impairment, most will develop hypertension during pregnancy with an associated increase risk of pre-eclampsia (30%), pre-term delivery and potential deterioration in renal function (20%). The maternal renal outlook is often worse in patients with reflux nephropathy and urinary infection should be screened for and treated. Despite this the fetal outcome is usually good with less than 10% fetal loss.

ECG changes in hyperkalaemia

The presence of tall, peaked T waves, flattened P waves, prolonged PR interval and wide QRS complexes are pathognomonic of hyperkalaemia. Give IV calcium immediately (10mls, 10% calcium gluconate) and call the renal team.

Hyperkalaemic distal renal tubular acidosis secondary to tacrolimus

Hyperkalaemia can be a problem post transplant. There are many causes to consider. In this case the notable features are a hyperkalaemia associated with a metabolic acidosis but without evidence of renal failure, lactic acidosis or haemolysis. The patient was notably diabetic. Although enoxaparin can rarely be associated with hyperkalaemia, the presence of risk factors, a metabolic acidosis, and an inappropriately low urine pH is more in keeping with a distal renal tubular acidosis. Tacrolimus has been well described to cause this.

Phosphate homeostasis

There is now good data that elevated serum phosphate levels are associated with increased cardiovascular risk.

CAPD is not as efficient at clearing phosphate as haemodialysis.

The stimuli to PTH secretion are low serum calcium concentration, low vitamin D levels and elevated phosphate levels.

Vitamin D increases calcium absorption from the gut: it does not lower blood phosphate concentration.

Phosphate binders should be taken just before meals so that they are present in the gut and available to bind phosphate when required.

Post-operative Renal Impairment

Fig 1: Kidney

Post-operative declines in renal function are common and can be triggered by many factors including hypotension, sepsis and drug effects, especially those of non-steroidal anti-inflammatory drugs and aminoglycosides. However, low dose prednisolone is not a cause of renal impairment.

Renal tubules

Frusemide acts on the Na+K+2Cl- cotransporter in the thick ascending limb of Henle's loop.
Thiazides act mainly on the Na+Cl- cotransporter in the distal convoluted tubule.
Parathyroid hormone decreases phosphate reabsorption by the kidney.
Renin is produced by the juxta glomerular apparatus.