Acute kidney injury and chronic kidney disease

The kidney defends its own filtration within a range of pressures. Arteriolar autoregulation adjusts the tone of the afferent and efferent arterioles so that glomerular pressure, and therefore the filtration rate, stays stable while mean arterial pressure moves between roughly 80 and 180 mmHg. Below that range the defence fails: renal blood flow falls, and the tubules, which are the most oxygen-hungry part of the kidney, become ischaemic. The same tubular cells that were reabsorbing sodium now leak it, their brush border is lost, and dead cells are shed into the urine as granular casts — the sediment that tells the clinician the injury has moved from prerenal to intrarenal. The distinction matters because the treatment is opposite. A purely prerenal kidney is conserving sodium avidly: urine sodium is low, the urine is concentrated, and the blood urea rises out of proportion to creatinine, so the urea-to-creatinine ratio is high. Once acute tubular necrosis is established, the tubule can no longer conserve sodium, urine sodium rises, and the fractional excretion of sodium becomes a useful discriminator. It is also here that a common teaching needs correcting: the rule that acute renal failure gives a low urine specific gravity is true only once tubular function has been lost. In the prerenal phase the urine is concentrated, with a high specific gravity and osmolality, because the kidney is working hard to hold water. Oliguria, conventionally fewer than 400 mL of urine in 24 hours, and anuria, less than about 100 mL, are the bedside signals, but a patient can also have a non-oliguric injury with a normal volume and a rising creatinine. The treatment arsenal is aimed at flow and at the fluid column: restoring volume and pressure, stopping the offending drug, and using loop diuretics such as furosemide or ethacrynic acid, or an osmotic agent such as mannitol, when a diuresis is prescribed — remembering that these drugs change urine volume without themselves repairing the tubule.

Not every damaged kidney is poisoned or starved by a general fall in blood pressure; sometimes the vessels themselves are the disease. Renal vascular disease affects the blood flowing into and out of the kidneys and can cause kidney damage, kidney failure and hypertension. Renal artery stenosis is a narrowing or blockage of an artery to a kidney. Smokers are at greater risk, and it is commonest in men between 50 and 70; high cholesterol, diabetes, excess weight and a family history of heart disease also raise the risk. An important point is that high blood pressure is both a cause and a result of stenosis, and the mechanism explains why: reduced flow to the kidney is sensed as a threat to volume, so the kidney releases renin and the renin–angiotensin–aldosterone system raises pressure. The classic clues are hypertension that does not improve with three or more medicines, a raised urea, unexplained kidney failure, and sudden kidney failure when an angiotensin-converting enzyme inhibitor is started — because when both renal arteries are narrowed, or the artery to a solitary functioning kidney is narrowed, the angiotensin II that constricts the efferent arteriole is what keeps glomerular pressure up, so blocking it can precipitate acute kidney injury.

Renal artery thrombosis is a clot in an artery supplying the kidney; it presents abruptly with flank pain, fever, blood in the urine, nausea and vomiting, a sudden fall in function and hypertension, though a gradual clot may be silent. Renal vein thrombosis is a clot in the draining vein: slow onset usually causes no symptoms, while sudden onset gives severe flank pain with spasms, tenderness over the kidney, declining function and blood in the urine, and it is treated with an anticoagulant given intravenously for several days and then orally. A renal artery aneurysm is a weak, bulging arterial wall that usually causes no symptoms but may cause hypertension or, if it tears, flank pain and haematuria; because of the rupture risk it is generally repaired in a pregnant woman or one of childbearing age. Atheroembolic renal disease occurs when a fragment of plaque breaks off a larger artery and blocks small renal arteries; it is increasingly common in older adults, and it announces itself with skin lesions or a reddish-purple discoloration, discoloured toes and feet, kidney failure, abdominal pain, diarrhoea, confusion, weight loss, fever and muscle aches.

Diagnosis uses an arteriogram or angiogram, duplex ultrasound, renography, or magnetic resonance angiography, and treatment ranges from blood pressure medicines other than angiotensin-converting enzyme inhibitors, cholesterol-lowering drugs and diabetes control through angioplasty, stenting and bypass surgery to thrombolytic infusion for an acute arterial clot. Left untreated, renal vascular disease can progress to kidney failure requiring dialysis or transplantation and is complicated by heart disease, stroke, myocardial infarction, heart failure, vascular damage and loss of vision.

Because retained waste circulates everywhere, uraemia reads like a list of unrelated complaints until each one is connected to its mechanism. Neurologically the patient is weak and tired, cannot concentrate, becomes confused or disoriented, and may develop tremors, restless legs, a burning sensation in the soles or behaviour changes; in advanced disease these progress to seizures, which is why any twitching, headache or delirium is reported at once and treated with intravenous diazepam or phenytoin.

The skin becomes dry and flaky, itches intensely, bruises easily and produces thin brittle nails, because uraemic toxins are deposited in the tissues; cool bathing, frequent turning, moisturisers and trimmed fingernails prevent the excoriation that scratching causes. Cardiovascularly, hypertension, pitting oedema of the feet, hands and sacrum, periorbital oedema and engorged neck veins reflect sodium and water retention, and the pericardium becomes inflamed, sometimes with an effusion, when waste retention is combined with inadequate dialysis. Hyperkalaemia and hyperlipidaemia are common, and hypertension is sustained both by volume overload and by malfunction of the renin–angiotensin–aldosterone system. In the lungs, thick tenacious sputum, a depressed cough reflex, pleuritic pain, breathlessness and tachypnoea are the price of fluid retention and uraemic irritation. The gastrointestinal tract gives an ammonia odour to the breath, described as uraemic fetor, a metallic taste, mouth ulcerations and bleeding, anorexia, nausea, vomiting, hiccups, constipation or diarrhoea, and bleeding that is worsened by platelet dysfunction.

Haematologically there is anaemia, which arises from inadequate erythropoietin production, a shortened red cell lifespan, nutritional deficiencies and bleeding, together with a low platelet count; recombinant human erythropoietin is given intravenously or subcutaneously three times a week, and because the haematocrit takes two to six weeks to rise it is not the answer for a patient who needs immediate correction of severe anaemia. Reproductively, women develop amenorrhoea and men testicular atrophy, infertility and reduced libido. In the skeleton, muscle cramps and loss of strength accompany renal osteodystrophy, bone pain and fractures, driven by retained phosphate, low serum calcium, abnormal vitamin D metabolism and, historically, aluminium accumulation, with metastatic and vascular calcification as a further consequence. Phosphate and calcium binders such as calcium carbonate or calcium acetate are given with meals, at the risk of hypercalcaemia; seizures are controlled with diazepam or phenytoin; heart failure and pulmonary oedema are treated with fluid restriction, a low-sodium diet, diuretics, inotropic agents such as digoxin or dobutamine, and dialysis; and nutrition aims at adequate calories, controlled protein, fluid, sodium and potassium, with vitamin supplementation.

Why prevention matters is plain: mortality in acute renal failure ranges from 25 to 90 per cent and is influenced by increased age, comorbid conditions and pre-existing renal and vascular disease. Four prevention principles follow from the causes. First, protect the circulating volume: give adequate hydration to patients at risk of dehydration, and treat shock promptly with blood and fluid replacement rather than waiting for the creatinine to move. Second, watch the numbers that change first: central venous and arterial pressures and hourly urine output in critically ill patients detect the onset of renal failure earlier than a daily laboratory result, and hypotension is treated promptly rather than observed. Third, keep the kidney out of the way of other treatment: confirm that the right blood is given to the right patient, because a severe transfusion reaction can precipitate renal failure; prevent and treat infection promptly, since infection can produce progressive renal damage; pay special attention to wounds, burns and other precursors of sepsis; give meticulous care to indwelling catheters and remove them as soon as possible so that infection does not ascend the urinary tract; and monitor the dose, duration and blood levels of every drug metabolised or excreted by the kidneys.

Once injury is established, the nursing priorities are fluid and electrolyte balance — electrolyte levels, physical signs of imbalance, careful selection of intravenous solutions, and screening of all oral intake and medicines for hidden potassium — together with daily weight and strict intake and output records. Rest reduces the metabolic rate during the acute phase, and fever and infection are prevented or treated because both increase catabolism. Pulmonary function is protected by turning, coughing and deep breathing to prevent atelectasis and respiratory infection, and asepsis with invasive lines and catheters limits infection risk. Skin care matters because the skin may be dry or oedematous and because deposited toxins cause itching and excoriation; cool bathing, frequent turning, clean well-moisturised skin and trimmed nails are both comforting and preventive.

Finally, psychosocial support and repeated explanation matter, because a patient who may need haemodialysis is anxious and frightened, and the family needs the same information. Nutritional therapy addresses the catabolism directly: the patient is weighed daily and should lose 0.2 to 0.5 kg per day while in negative nitrogen balance, so gaining weight, failing to lose weight or developing hypertension suggests fluid retention; calories come mainly from carbohydrate because of its protein-sparing effect, and foods rich in potassium or phosphorus, such as bananas, citrus fruit and coffee, are restricted.