21.3 — Kidney Disease

You can lose most of your kidney function and feel completely well.

Symptoms typically appear only when function falls below around 15 percent of normal, by which point the damage is permanent and the conversation is about dialysis and transplantation.

Which is why chronic kidney disease is found on a blood test rather than by how someone feels, and why that test is one of the highest-value routine measurements in medicine.

Around 10 percent of adults worldwide have chronic kidney disease, and most do not know.

Measuring kidney function

eGFR — estimated glomerular filtration rate. How much fluid the kidneys filter per minute, estimated from blood creatinine, age and sex (Chapter 10.2).

Normal is above 90. Below 60 for more than three months defines chronic kidney disease.

Creatinine is a waste product of muscle, which is why the estimate is adjusted — and why a very muscular person can have a high creatinine with normal kidneys, and why someone with little muscle mass can have a normal-looking creatinine with poor kidney function. Cystatin C is used when the estimate is doubtful.

Urine albumin-to-creatinine ratio. Protein leaking into the urine is a sign the filter is damaged, and it is measured because it predicts progression and cardiovascular risk independently of the eGFR.

Both tests together define the stage, and both matter — someone with a normal eGFR and significant protein leak is at real risk.

Chronic kidney disease

Causes

Diabetes is the leading cause worldwide (Chapter 18.7). High glucose damages the small vessels of the filtering units, and the first sign is protein appearing in the urine.

High blood pressure is the second, and the relationship runs both ways: hypertension damages kidneys, and damaged kidneys raise blood pressure, because the kidney controls fluid volume and produces renin (Chapter 10.3). Which makes it a loop that has to be interrupted deliberately.

Glomerulonephritis — a group of conditions where the filtering units are inflamed, often immune-mediated.

Polycystic kidney disease — inherited, with cysts progressively replacing kidney tissue. Autosomal dominant, so children of an affected parent have a 50 percent chance (Chapter 2.6).

Obstruction — from an enlarged prostate, stones, or tumours. Important because it is potentially reversible if relieved in time.

Drugs — NSAIDs taken regularly, particularly with dehydration or in older people; some antibiotics; and contrast agents.

Recurrent infection and repeated episodes of acute kidney injury.

What goes wrong as function falls

And each of these follows directly from something the kidney does (Chapter 10.3), which makes them easy to remember rather than a list to memorise.

Waste accumulates — urea and other products, causing nausea, itching, poor appetite and fatigue.

Fluid accumulates — swelling of the legs, and eventually of the lungs.

Potassium rises — and this is the dangerous one, because high potassium causes fatal heart rhythm disturbances (Chapter 7.3).

Acid accumulates, because the kidney normally excretes it.

Anaemia, because the kidney makes erythropoietin, the hormone that tells the bone marrow to make red cells (Chapter 7.1). Treated with erythropoietin-stimulating agents and iron.

Bone disease, because the kidney performs the final activation step for vitamin D, so calcium absorption falls, parathyroid hormone rises, and bone is broken down (Chapter 12.3).

And accelerated cardiovascular disease — which is what most people with chronic kidney disease actually die of, rather than kidney failure itself. Someone with kidney disease is at far higher cardiovascular risk than kidney risk, which is why treating blood pressure and cholesterol is part of kidney care.

Treatment

And this section has genuinely changed in the last few years, which is why the chapter is optimistic.

Blood pressure control — the foundation. ACE inhibitors or ARBs are preferred where there is protein in the urine, because they reduce pressure inside the filtering unit specifically and slow progression beyond their effect on blood pressure alone.

SGLT2 inhibitors, and these are the significant development.

Originally developed as diabetes drugs, they turned out to slow kidney disease progression substantially — and in people without diabetes as well. They reduce the risk of kidney failure and of cardiovascular death, and they are now standard for chronic kidney disease with protein in the urine regardless of diabetes status.

Finerenone — a mineralocorticoid receptor antagonist with additional benefit in diabetic kidney disease.

Glucose control in diabetes.

Treating cholesterol.

Avoiding harm — NSAIDs, and adjusting doses of drugs cleared by the kidney.

Sick day rules, and this is a practical thing worth knowing: during vomiting, diarrhoea or fever, certain medications are temporarily paused — ACE inhibitors, ARBs, diuretics, metformin, SGLT2 inhibitors and NSAIDs — because dehydration plus these drugs is a common route into acute kidney injury. Anyone taking them should know this and should have been told.

Diet — moderating salt, and potassium and phosphate restriction in advanced disease. Protein restriction is used cautiously, because malnutrition carries its own risks.

And planning ahead in advanced disease — creating dialysis access, assessing for transplant, or choosing conservative management, all of which go better when decided in advance rather than in a crisis.

Acute kidney injury

A sudden fall in kidney function over hours to days.

Very common in hospital, affecting perhaps 10 to 20 percent of inpatients, and frequently preventable.

Three categories, and the division is genuinely useful because it points at the treatment:

Before the kidney — reduced blood flow. Dehydration, bleeding, heart failure, sepsis, or drugs that reduce kidney perfusion. The commonest cause, and the most reversible.

In the kidney — direct damage from toxins, drugs, or inflammation of the kidney tissue.

After the kidney — obstruction to urine flow. Always considered, because relieving it can restore function completely — and a blocked catheter or an enlarged prostate is an easy thing to miss and an easy thing to fix.

Signs: reduced urine output, swelling, confusion, nausea, and rising creatinine on blood tests.

Treatment: restore fluid balance, stop the offending drugs, relieve obstruction, treat infection, and dialysis if needed temporarily.

Most people recover, and an episode of acute kidney injury increases the long-term risk of chronic kidney disease, so follow-up afterwards matters.

Kidney stones

Affecting around 10 percent of people at some point, and more in hot climates and in men.

Renal colic is described as among the most severe pains there is — sudden, severe, in the flank, radiating to the groin, coming in waves, with the person unable to find a comfortable position.

And that restlessness is a useful sign, because someone with peritonitis lies perfectly still while someone with colic paces.

With nausea, vomiting, and blood in the urine, often visible only on testing.

Types: calcium oxalate is the commonest; then uric acid; struvite stones, which form in association with certain urinary infections and can grow very large; and cystine stones from an inherited transport defect.

Treatment of the attack: NSAIDs are more effective than opioids for renal colic, which is a well-established and frequently surprising finding. Fluids and antiemetics.

Most stones under 5 millimetres pass on their own. Larger ones may need lithotripsy — shock waves breaking the stone — or ureteroscopy.

And an emergency to recognise: an obstructing stone with infection. Fever plus obstruction is a urological emergency needing urgent drainage, because the infection behind an obstruction becomes overwhelming quickly.

Prevention, and it works:

Fluid, and this is by far the most effective measure. Aim for around 2.5 litres of urine a day, which for most people means drinking around 3 litres.

Reducing salt, which increases calcium excretion.

Moderate calcium intake — and counter-intuitively, restricting dietary calcium increases stone risk, because calcium in the gut binds oxalate and prevents its absorption. So low-calcium diets for calcium stones are wrong.

Reducing oxalate-rich foods in oxalate stone formers, and reducing animal protein.

Citrate, which inhibits crystal formation — from lemon juice or potassium citrate.

Urinary tract infection

Very common, particularly in women, because the urethra is short (Chapter 10.5).

Cystitis — burning on passing urine, frequency, urgency, and lower abdominal discomfort.

Pyelonephritis — infection reaching the kidney. Fever, loin pain, and feeling systemically unwell. This is the serious one, and it needs prompt antibiotics and sometimes admission.

Treatment: short-course antibiotics for simple cystitis — nitrofurantoin or trimethoprim commonly, guided by local resistance patterns. Longer courses and different antibiotics for kidney involvement.

Investigate when: it occurs in men, recurs frequently, involves the kidney, or occurs in pregnancy — where even symptomless bacteria in the urine are treated, because of the risk of pyelonephritis and preterm birth.

Prevention for recurrent infection: fluids — and a trial found that increasing water intake by 1.5 litres a day halved recurrences, which is a remarkably simple result. Also urinating after sex, avoiding spermicides, vaginal oestrogen after menopause, which has good evidence, and D-mannose or cranberry with weaker evidence.

And a caution: bacteria in the urine without symptoms is common in older people and usually should not be treated, because treating it produces resistance without benefit. Confusion alone in an older person is not sufficient reason to diagnose a urinary infection, and doing so routinely means the real cause gets missed.

Dialysis and transplantation

Haemodialysis — blood pumped through a filter, usually three times a week for around four hours, requiring vascular access created in advance.

Peritoneal dialysis — using the lining of the abdomen as the filter, done at home, daily, offering more independence.

Transplantation is the better treatment where it is possible — better survival, better quality of life, and lower cost than long-term dialysis.

Living donation gives better outcomes than deceased donation, and a person can live a normal life with one kidney, with the remaining kidney enlarging to compensate.

Requires lifelong immunosuppression, with its own risks — infection and increased cancer risk.

And the good news is real: transplant outcomes have improved steadily, with most kidneys functioning well many years later.

What is worth doing

If you have diabetes or high blood pressure, have your kidney function and urine protein checked regularly. That is the whole prevention strategy for the majority of cases.

Drink enough water.

Do not take NSAIDs regularly without knowing your kidney function.

Know the sick day rules if you take the relevant medications.

And treat blood pressure seriously, because it is the single largest modifiable factor for both kidneys and everything else.

What the next page fixes

Chapter 21.4 covers thyroid and the other endocrine diseases — conditions that are commonly missed because their symptoms look like ordinary life, and that respond very well once found.