Nephrology Department

What our nephrology unit covers — and who it is for

Nephrology is the medical care of the kidneys: what damages them, how far the damage has gone, how to slow it, and what to do when they can no longer do the job. It is a medical specialty, not a surgical one. Kidney stones, obstruction and the prostate belong to urology; the transplant operation itself is performed by transplant surgery, and the dialysis fistula is created by vascular surgery. Everything either side of those operations is nephrology.

At Acıbadem International the work is organised into five strands.

• Chronic kidney disease — establishing the stage, finding the cause, and slowing the decline, which is the largest part of the workload by a distance.
• Glomerular disease — the immune and inflammatory diseases of the filters themselves, diagnosed by kidney biopsy and treated with immunosuppression.
• Acute kidney injury — sudden loss of function in hospital or after a drug, procedure or illness, where most of the work is stopping what is causing it.
• Dialysis — haemodialysis, peritoneal dialysis and home therapies, including the decision of when to start and which to choose.
• Transplantation, medically — candidacy, work-up, immunosuppression and rejection, before and after the operation.

What a nephrologist actually does — the kidney doctor

A nephrologist is the kidney doctor, and most people are referred to one for a number rather than a symptom — a creatinine that has drifted up, protein found on a urine dipstick, an eGFR printed on a routine blood test. Kidney disease is largely silent until it is advanced, which is why it is usually found by measurement rather than by how someone feels.

The consultation therefore answers four questions in order. How much function is there, measured rather than guessed. Is this acute or chronic — a distinction that changes everything, because acute loss is often reversible and chronic loss is not. What caused it, because treating the cause is the only thing that alters the trajectory. And how fast is it moving, which decides whether anything needs planning now.

Two things follow that patients rarely expect. Most of what a nephrologist prescribes is not a kidney drug — it is blood pressure control, glucose control and the medicines that protect the kidney indirectly, because those are what actually slow decline. And a large part of the job is subtraction: stopping or adjusting the medicines that are harming the kidney, which is frequently the single most effective intervention available.

Chronic kidney disease

Chronic kidney disease is a reduction in kidney function, or evidence of kidney damage, that has been present for more than three months. That three-month qualifier is the whole difference between this and acute kidney injury, and it is why a single abnormal blood test is not a diagnosis.

It is common, it is under-diagnosed, and it is usually silent. Symptoms — fatigue, poor appetite, itching, swelling, breathlessness, disturbed sleep — appear late, and by the time they do a great deal of function has gone. That is the argument for measurement in the groups where it is likely: diabetes, hypertension, cardiovascular disease, family history, and long-term use of drugs that affect the kidney.

The most important thing to say about it is also the least dramatic. The purpose of treatment in most people is not to restore function but to slow the slope — and the slope matters enormously, because someone losing function slowly may never need dialysis in their lifetime while someone losing it quickly will. Almost everything in this section exists to bend that line.

CKD stages, kidney disease stages and what eGFR means

CKD stages — the kidney disease stages — are defined by the estimated glomerular filtration rate, and this section is the only place on this page where the classification is set out; other sections refer back to it.

• Stage 1 — eGFR 90 or above, with evidence of kidney damage such as protein in the urine. Normal filtration, abnormal kidney.
• Stage 2 — eGFR 60 to 89, again with evidence of damage. A reduced eGFR alone at this level, with no protein and no structural abnormality, is not kidney disease.
• Stage 3a — eGFR 45 to 59, and stage 3b — eGFR 30 to 44. This is where most people are found and where most of the treatment happens.
• Stage 4 — eGFR 15 to 29. Planning for what comes next begins here, well before it is needed.
• Stage 5 — eGFR below 15, described as kidney failure, at which dialysis or transplantation is considered.

Two qualifications matter. Staging is completed by the amount of protein in the urine, not by eGFR alone, because two people at the same eGFR with very different protein levels have very different outlooks — the protein is often the better predictor of the two. And an eGFR is an estimate calculated from creatinine, age and sex; it performs poorly at the extremes of muscle mass, which is why cystatin C, produced independently of muscle, is used to confirm the picture where the creatinine-based estimate is unreliable.

The number people fixate on is the stage. The number that predicts their future is the rate of change, which is why the trend across several tests is more informative than any single result.

Kidney function test: creatinine, BUN, cystatin C, albumin creatinine ratio, microalbuminuria and proteinuria

A kidney function test is a panel rather than one measurement, and knowing what each part does removes most of the confusion when the results arrive.

Creatinine is a waste product of muscle, cleared by the kidney, so it rises as filtration falls. Its weakness is that it depends on how much muscle you have — a muscular young man and a frail elderly woman with the same creatinine have very different kidney function, which is why the raw number is less useful than the estimate derived from it. BUN, blood urea nitrogen, rises with reduced filtration but also with dehydration, bleeding into the gut and a high protein intake, so it is read alongside creatinine rather than alone.

The urine tells you more about the kidney than the blood does. The albumin creatinine ratio on a single urine sample quantifies protein leak, and it is the test that both stages the disease and predicts its progression. Microalbuminuria, now more often called moderately increased albuminuria, is the earliest detectable leak and the point at which treatment changes outcomes most. Proteinuria at higher levels points toward disease of the filters themselves and is what prompts a biopsy discussion.

An ultrasound completes the initial picture: kidney size, obstruction, cysts, and whether the kidneys look scarred and shrunken, which itself distinguishes chronic from acute.

Haematuria (hematuria): blood in the urine

Hematuria divides into two problems that share an appearance and go to two different specialties, and getting the division right is the whole of the initial assessment.

Visible blood — urine that is pink, red or brown — is a urological question until proven otherwise, because the concern is a tumour of the bladder or kidney, a stone, or infection. It is investigated with imaging and cystoscopy by urology, and painless visible haematuria in an adult is never dismissed.

Non-visible blood, found on a dipstick, is a nephrological question when it comes with protein, with raised blood pressure or with reduced function — that combination points to the glomeruli, and the red cells seen under the microscope are misshapen because they have been forced through a damaged filter. That is the picture that leads to glomerulonephritis and to a biopsy. Non-visible blood alone, with no protein and normal function, is investigated to exclude urological causes and then followed rather than pursued indefinitely.

Acute kidney injury

Acute kidney injury is a sudden fall in kidney function over hours to days. It differs from chronic disease in the one respect that matters most: it is frequently reversible, and how completely depends largely on how quickly the cause is removed.

The causes are grouped by where the problem sits relative to the kidney, and the grouping is genuinely useful rather than academic. Before the kidney — inadequate blood reaching it, from dehydration, blood loss, sepsis, heart failure or the drugs that drop perfusion. In the kidney — damage to the tissue itself from prolonged low perfusion, from drugs, from contrast, or from an inflammatory disease. After the kidney — obstruction to the outflow, from stones, an enlarged prostate or a pelvic mass, which is the group that is completely reversible if relieved in time and is why an ultrasound is done early.

Treatment is mostly subtraction and support: restoring circulating volume where it is depleted, relieving obstruction where it is present, stopping the drugs contributing to it, and treating the underlying illness. Dialysis in this setting is temporary support while the kidney recovers, not a permanent commitment — and in intensive care it is often given continuously rather than intermittently, as continuous renal replacement therapy, because a patient with unstable blood pressure tolerates slow steady clearance far better than a short intense session.

One consequence is frequently not explained. An episode of acute kidney injury that appears to resolve completely still raises the long-term risk of chronic kidney disease, which is why function is rechecked months later rather than assumed to have returned to baseline.

Contrast induced nephropathy and drugs that harm the kidney

Contrast induced nephropathy is a rise in creatinine after intravenous iodinated contrast for a CT or angiogram. Its importance has been revised downward in recent years — much of what was attributed to contrast in older studies reflected how unwell the patients already were — but the risk is real in those with pre-existing chronic kidney disease, diabetes and dehydration. Prevention is unglamorous and effective: adequate hydration before and after, using the smallest necessary volume of contrast, and reviewing the other nephrotoxic drugs around the same time. A scan that is genuinely needed is not withheld because of it.

The drugs that harm the kidney are worth naming because so many are bought without prescription. Non-steroidal anti-inflammatory drugs reduce the blood flow the kidney depends on, and the risk rises sharply in dehydration, in older people and in combination with other drugs acting on the same pathways. Some antibiotics, some antiviral drugs, some chemotherapy agents and certain herbal preparations are also implicated. The rule is not that these drugs are forbidden — it is that in someone with reduced kidney function they are prescribed, dosed and monitored deliberately by the doctor responsible, and that includes anything bought over the counter, which is worth mentioning at every appointment.

Glomerulonephritis and glomerular disease

Glomerulonephritis — often shortened to nephritis — is inflammation of the glomeruli, the million-odd microscopic filters in each kidney. It is not one disease but a family of them, and they are distinguished by what a biopsy shows rather than by symptoms, because the presentations overlap almost completely.

Two patterns describe how they present, and the distinction organises the whole field. Nephritic presentations are inflammatory: blood in the urine with misshapen red cells, moderate protein leak, raised blood pressure and falling function. Nephrotic presentations are leaky rather than inflamed: heavy protein loss, low blood albumin and swelling, with function often preserved at first. Many diseases can produce either, and some produce both.

What matters practically is that these are the kidney diseases where treatment can change the outcome substantially, and where delay costs function that does not come back. That is why a rising creatinine with blood and protein in the urine is investigated quickly rather than watched.

Nephrotic syndrome

Nephrotic syndrome is defined by the combination of heavy protein loss in the urine, low albumin in the blood, and swelling — typically around the eyes in the morning and in the legs by the evening — often with raised cholesterol. It is a syndrome rather than a diagnosis: the job is to find which disease is producing it.

Two complications deserve stating because they are what makes it more than an inconvenience. Loss of proteins that regulate clotting leaves the blood prone to clotting, and the risk of venous thrombosis is genuinely raised. And loss of immunoglobulins leaves patients more susceptible to infection. Both are managed actively rather than watched.

In adults the cause is established by kidney biopsy in almost all cases — membranous nephropathy, FSGS, minimal change disease, diabetic disease and amyloid being the common answers. In children the pattern is different enough that treatment is frequently started without a biopsy, because minimal change disease dominates and responds to steroids.

IgA nephropathy

IgA nephropathy is the commonest primary glomerulonephritis worldwide. Abnormally formed IgA antibody deposits in the glomeruli and provokes inflammation, and the classical presentation is visible blood in the urine appearing within a day or two of a throat or respiratory infection — a timing that distinguishes it from the post-infectious nephritis that follows weeks later.

Its course is the honest difficulty with it. Many people do well for decades; a substantial minority progress to kidney failure over twenty to thirty years, and predicting which group someone is in is imperfect. The predictors that matter are the amount of protein in the urine, the blood pressure, the function at diagnosis and the degree of scarring on biopsy.

Treatment begins with the measures that protect any kidney — blood pressure control, blockade of the renin-angiotensin system, and reduction of protein leak — and immunosuppression is added in those with persistent protein loss despite that. Newer targeted treatments have changed this area recently, and what applies to an individual is decided by the treating nephrologist rather than from a general account.

Membranous nephropathy

Membranous nephropathy is a leading cause of nephrotic syndrome in adults, in which immune complexes deposit along the outside of the filtering membrane and thicken it. Most cases are primary and driven by an antibody against a specific podocyte protein, PLA2R — an antibody measurable in the blood, which has genuinely changed practice: it supports the diagnosis without a biopsy in some cases and, more usefully, tracks the disease so that treatment response can be followed with a blood test.

A minority are secondary — to malignancy, to hepatitis B, to lupus, or to drugs — and that is why an adult with membranous disease is screened for an underlying cause rather than treated immediately as primary. The course is famously variable: a proportion remit spontaneously, a proportion remain stable with protein leak, and a proportion progress. Because of that, low-risk patients are treated conservatively for a period first, and immunosuppression is reserved for those with persistent heavy protein loss or declining function.

FSGS: focal segmental glomerulosclerosis

FSGS is scarring affecting some glomeruli and only part of each affected one, which is what focal and segmental describe. It presents with nephrotic syndrome or with protein leak and declining function, and it matters because it is one of the more difficult glomerular diseases to treat.

The critical distinction is between primary FSGS — an immune-mediated attack on the podocytes, which is treated with immunosuppression — and secondary FSGS, in which the pattern of scarring results from the remaining glomeruli being overworked, in obesity, in reflux nephropathy, after loss of kidney mass, or with certain drugs. Secondary FSGS does not respond to immunosuppression and treating it that way exposes someone to serious drug toxicity for no benefit, which is why the distinction is made on the biopsy and the clinical picture together rather than on the pattern alone. Genetic forms exist and are increasingly identified, particularly in younger patients and in those of African ancestry, where APOL1 variants raise the risk substantially.

Minimal change disease

Minimal change disease is named for what the biopsy shows under a standard microscope, which is nothing — the abnormality is visible only on electron microscopy, as flattening of the podocyte foot processes. It is the commonest cause of nephrotic syndrome in children and a recognised cause in adults.

Its behaviour is the opposite of FSGS: it responds well to steroids in the great majority, often completely. The difficulty is relapse rather than resistance — many patients relapse when treatment is reduced, and repeated courses of steroids carry their own cost, which is why steroid-sparing agents are used in those who relapse frequently. In adults it responds more slowly than in children, and an adult who has not responded by the expected point is reassessed rather than simply given more.

Lupus nephritis

Lupus nephritis is kidney involvement in systemic lupus erythematosus, and it develops in a substantial proportion of people with lupus — often early, and frequently without symptoms until it is advanced. That silence is why urine testing at every lupus review is not a formality: protein or blood appearing on a dipstick is often the first sign, and it appears long before anyone feels unwell.

Biopsy is central here in a way it is not in every glomerular disease, because lupus nephritis is divided into six classes with very different treatments — some requiring aggressive immunosuppression, others requiring almost none — and the class cannot be predicted from blood tests. Repeat biopsy is sometimes needed because the class can change over time.

Treatment is intense immunosuppression in the proliferative classes, with an induction phase and then a long maintenance phase, and the two commonest reasons for a poor outcome are late diagnosis and stopping maintenance treatment early. The lupus itself is managed alongside internal medicine and rheumatology; the kidney is managed here, and the two run together.

Kidney biopsy

A kidney biopsy takes small cores of kidney tissue with a needle through the back, under ultrasound guidance and local anaesthetic, and it is the only way to establish what most glomerular diseases actually are. It is not done to confirm what is already obvious — long-standing diabetes with a typical picture and small scarred kidneys does not need one — but it is done whenever the diagnosis would change the treatment.

What people want to know is the risk. The significant one is bleeding, since the kidney is a highly vascular organ; most bleeding is minor and self-limiting, a small proportion need a transfusion, and a very small proportion need a procedure to stop it. That is why clotting is checked, blood pressure is controlled and blood-thinning medicines are held beforehand by the doctor prescribing them, and why patients are observed with monitoring for several hours afterwards.

The tissue is examined three ways — light microscopy, immunofluorescence for antibody deposits, and electron microscopy for the fine structure — which is why the full result takes days rather than hours, and why a biopsy done where all three are available answers questions that one done with light microscopy alone cannot.

Diabetic nephropathy

Diabetic nephropathy — diabetic kidney disease — is the leading cause of kidney failure worldwide, and its course is well enough characterised that it can be intercepted. It begins with a period of raised filtration, then microscopic protein leak, then increasing protein loss with rising blood pressure, then declining function.

The point of that sequence is that the early stages are silent and detectable, which is the entire argument for annual urine albumin testing in everyone with diabetes. Intervening at the microalbuminuria stage changes the trajectory far more than anything available later.

What has changed this field is that the treatment is no longer only glucose and blood pressure. Blockade of the renin-angiotensin system reduces protein leak and slows progression. SGLT2 inhibitors, developed as diabetes drugs, have been shown to protect the kidney substantially — including in people without diabetes — and are now a mainstay. Non-steroidal mineralocorticoid receptor antagonists add further benefit in diabetic kidney disease. Which of these applies to an individual, at what dose and in what combination, is decided by the treating team, and the shift they represent is that diabetic kidney disease is now a treatable trajectory rather than an inevitable one. Diabetes itself is managed with endocrinology.

Polycystic kidney disease

Polycystic kidney disease is an inherited condition in which cysts form and enlarge throughout both kidneys over decades, gradually replacing working tissue. The autosomal dominant form is much the commonest and is one of the most frequent inherited diseases there is; each child of an affected parent has a one in two chance of inheriting it, which makes family screening a real conversation rather than a theoretical one.

It typically declares itself in adulthood — with high blood pressure, which is often the first sign and appears before function falls; with pain from cyst enlargement, bleeding into a cyst or infection; with blood in the urine; or with kidney stones. Function is usually preserved for a long period while the kidneys enlarge, and then declines, and total kidney volume on imaging predicts the trajectory better than eGFR does in the early years.

It is not only a kidney disease, and the extra-renal features are the reason it needs a nephrologist rather than a scan report. Cysts in the liver are very common and occasionally the dominant problem. Intracranial aneurysms occur at a higher rate than in the general population, which is why screening is offered where there is a family history of aneurysm or bleed. Heart valve abnormalities and diverticular disease occur more often.

Management is blood pressure control, generous fluid intake, and treatment of pain, infection and stones. A vasopressin receptor antagonist slows cyst growth and the decline in function in selected patients at high risk of rapid progression — it requires close monitoring of liver function and causes considerable thirst and urine output, and whether it is appropriate is an individual decision made by the treating nephrologist.

Kidney cyst and the Bosniak classification

A kidney cyst found on a scan done for something else is one of the commonest incidental findings in medicine, and the great majority are simple and harmless. A simple renal cyst has a thin smooth wall, contains clear fluid, has no solid component and needs nothing at all — it is not a precursor to anything and it does not need following.

The question is which cysts are not simple, and that is what the Bosniak classification exists to answer. It grades cystic lesions on CT or MRI by wall thickness, internal septations, calcification and — the feature that matters most — whether any part of it takes up contrast, since enhancement indicates living tissue with a blood supply. Category I and II lesions are benign and need no follow-up. Category IIF requires surveillance imaging. Category III carries a meaningful risk of malignancy and category IV is treated as cancer, both of which move the patient to urology.

Two practical points. Multiple simple cysts increasing with age are normal and are not polycystic kidney disease, which is a different pattern in different kidneys with a family history. And a cyst reported without a Bosniak category on a scan done without contrast has not been fully characterised — that is a reason to complete the imaging rather than to worry.

Electrolyte and acid-base problems

The kidney regulates the composition of the blood as much as it clears waste from it, and when it fails, the disturbances it produces are frequently what brings someone to hospital.

Hyperkalemia

Hyperkalemia — high potassium — is the one that kills. Potassium is excreted almost entirely by the kidney, so it accumulates as function falls, and it is aggravated by the very drugs used to protect the kidney, by potassium-sparing diuretics, and by dietary potassium. It is dangerous because it is silent until it disturbs the heart rhythm, and severe hyperkalaemia is treated as an emergency wherever it is found. In chronic disease it is managed by reviewing medication, by diet, and increasingly by potassium binders that allow the protective drugs to be continued rather than stopped — which matters, because stopping them to control potassium trades a short-term number for a long-term decline.

Hyponatremia

Hyponatremia — low sodium — is the commonest electrolyte abnormality in hospital, and it is a problem of water rather than of salt: there is too much water relative to sodium. It causes confusion, unsteadiness and, when severe or rapid, seizures. Its causes are numerous and the treatment differs completely between them, which is why the assessment centres on the person’s fluid status and on urine measurements rather than on the number alone. One thing is universal: correcting it too quickly causes serious neurological injury, so the rate of correction is controlled deliberately and is itself part of the treatment.

Metabolic acidosis

Metabolic acidosis develops as the kidney loses the ability to excrete acid and to regenerate bicarbonate. Chronic acidosis is not merely a number: it accelerates the loss of muscle and bone and appears to speed the decline in kidney function itself, which is why oral bicarbonate is given to correct it rather than left alone.

Renal tubular acidosis

Renal tubular acidosis is a different and more specific entity — acidosis caused by a defect in the tubules rather than by loss of filtration, with normal or near-normal eGFR. It comes in types distinguished by which part of the tubule is at fault and by the accompanying potassium level, and it matters because it causes stones, bone disease and growth failure in children, and because it is treatable once identified.

The complications of advanced kidney disease

As function falls, a predictable set of problems follows, and each is managed in its own right rather than waiting for dialysis to solve them.

Anaemia of kidney disease and erythropoietin

Anaemia develops because the kidney produces erythropoietin, the hormone that drives red cell production, and a failing kidney produces less of it. The result is fatigue and breathlessness attributed to age or to the kidney disease generally, when it is a specific and treatable deficiency. Treatment addresses iron first — absorption is impaired and losses are higher — and erythropoiesis-stimulating agents are added where iron alone is insufficient, with the target deliberately below normal, because pushing haemoglobin to a normal level in this population increases cardiovascular events rather than improving outcomes.

Renal osteodystrophy and secondary hyperparathyroidism

Renal osteodystrophy is the bone disease of chronic kidney failure, and it is the visible part of a wider disturbance of mineral metabolism that also affects the blood vessels. The sequence is worth following because each step explains the treatment.

The failing kidney cannot excrete phosphate, so phosphate rises. It also cannot activate vitamin D, so calcium absorption falls. Both changes drive the parathyroid glands to produce more hormone — secondary hyperparathyroidism — which pulls calcium out of bone to correct the blood level. Over years the bone weakens and fractures, and the calcium and phosphate deposit in the walls of arteries and in the heart valves, which is a large part of why cardiovascular disease dominates the outcome in kidney failure.

Treatment therefore works along that chain: dietary phosphate restriction, phosphate binders taken with meals to bind phosphate in the gut before it is absorbed, activated vitamin D, and drugs that suppress the parathyroid glands directly. Where the glands become autonomous and no longer respond, they are removed surgically. The single most common practical failure is binders taken at the wrong time — they work only when taken with food, and taken between meals they do nothing at all.

The renal diet, and the low potassium diet

The renal diet is one of the harder parts of living with kidney disease, and it is frequently taught as a list of forbidden foods when it is really four separate restrictions applied at different stages to different people.

Sodium is restricted in almost everyone with kidney disease, because it drives blood pressure and fluid retention, and most dietary sodium comes from processed food rather than the salt cellar. Potassium is restricted only when the blood level is actually high — a low potassium diet imposed on someone with normal potassium removes fruit and vegetables for no benefit, which is a genuinely common error. Phosphate is restricted in advanced disease, and the most useful advice is about additives rather than natural foods, because phosphate added to processed food is absorbed far more completely than the phosphate in meat, dairy or pulses. Protein is moderated in advanced disease before dialysis, and then increased again once dialysis starts, because dialysis removes protein — which is why advice that was right last year can be wrong this year.

Fluid restriction applies to people on dialysis and to those with fluid overload, not to everyone with kidney disease. The specific targets for any individual are set by the treating team with a renal dietitian, alongside nutrition and dietetics, and following a diet sheet found online rather than one prescribed is how people end up malnourished while trying to protect their kidneys.

Dialysis

Dialysis replaces the clearing function of the kidney. It does not replace the kidney: the hormonal functions — erythropoietin, vitamin D activation — still have to be supplied separately, which is why someone on dialysis remains under nephrological care rather than simply attending a machine.

The most common question is when it starts, and the answer has changed. Dialysis is no longer begun at a particular eGFR. It is begun when symptoms and biochemistry require it — fluid overload that will not respond to diuretics, potassium or acidosis that cannot be controlled, uraemic symptoms such as nausea, itching and confusion, or malnutrition from loss of appetite. Trials comparing earlier with later starts found no benefit to starting early, so the threshold is clinical rather than numerical, and someone at stage 5 who feels well and whose bloods are controlled is not started on a number alone.

What does happen well before then is preparation, and that is the part where delay causes real harm. Access takes months to be ready, transplant work-up takes months, and the choice between modalities deserves unhurried thought. Starting dialysis urgently through a neck catheter because nothing was arranged is a worse start than any planned route, and it is the single most avoidable failure in this pathway.

Haemodialysis (hemodialysis)

Hemodialysis pumps blood out of the body through a filter that removes waste and excess fluid, and returns it. In-centre treatment is typically three sessions a week of about four hours, and the time is not negotiable in the way people hope — clearance depends on it.

Two things dominate the experience and are worth knowing in advance. The first is the swing: waste and fluid accumulate between sessions and are removed rapidly during them, which is why many people feel washed out for hours afterwards and why blood pressure can drop during treatment. Removing a large volume quickly is what causes that, and it is the reason fluid restriction between sessions genuinely matters rather than being a rule for its own sake. The second is access, which is discussed below.

Home hemodialysis

Home hemodialysis changes the arithmetic considerably. Done at home, more frequently and often for longer or overnight, it produces gentler fluid removal, better blood pressure and phosphate control, fewer dietary restrictions and better quality of life in most series. It requires training, a suitable home, and usually a partner or carer, and it is under-offered — anyone facing dialysis should ask about it explicitly rather than waiting to be offered it.

Peritoneal dialysis

Peritoneal dialysis uses the lining of the abdomen as the filter. Fluid is run into the abdominal cavity through a permanent soft catheter, left to draw waste and water across the membrane, then drained and replaced. It is done by the patient at home — either as several manual exchanges through the day, or overnight by a machine while asleep.

Its advantages are real and often undersold: no needles, no three-times-weekly travel, gentler continuous fluid removal that preserves remaining kidney function longer, a more liberal diet and fluid allowance, and far more independence for people who work or travel. Its limitations are equally real. Peritonitis is the main complication and is why the sterile technique training is taken so seriously. The membrane changes over years and can eventually stop working adequately, which means most people on it will move to haemodialysis at some point. And it is unsuitable after extensive abdominal surgery or with large hernias.

The honest framing is that these are not better and worse options but different lives, and the choice belongs largely to the patient once the medical constraints are set out.

Dialysis access

Dialysis access determines more about someone’s life on haemodialysis than almost anything else, and it is created long before it is used. The three options are not equivalent.

An arteriovenous fistula — an artery joined to a vein in the arm, which then enlarges and thickens over weeks — is the best access there is, with the lowest infection rate and the longest life. It is created by vascular surgery months before dialysis is expected, because it needs time to mature. A graft, using synthetic tubing, is the alternative where the veins are inadequate. A tunnelled neck catheter works immediately and is the worst option long term, with the highest rate of infection and of vein damage — it is for people who need dialysis before anything else is ready.

One instruction follows from all of this and is worth acting on years early: protect the forearm veins in anyone approaching kidney failure. Cannulas, blood tests and drips go elsewhere — ideally the back of the hand or the other arm — because a vein damaged by routine use cannot later become a fistula.

Kidney transplantation, medically

Kidney transplant is the best treatment for kidney failure for those who are suitable — better survival, better quality of life and fewer restrictions than dialysis. The operation is performed by transplant surgery; what belongs here is everything either side of it.

The point most often missed is timing. A transplant performed before dialysis has started — pre-emptive transplantation — produces better outcomes than one performed after years on dialysis. That means the work-up should begin while someone is still in stage 4, not when they are already on a machine, and late referral is the commonest reason a suitable candidate does not get a pre-emptive transplant.

Living donor kidney transplant offers the best results of all: better graft survival, a planned operation rather than an urgent one, and no waiting list. The evaluation of a potential donor is thorough and independent, and donors are followed long term afterwards, because the decision to remove a healthy kidney from a healthy person is taken with unusual care.

Candidacy assessment covers cardiac and vascular fitness, infection and malignancy screening, dental and urological assessment, and immunological testing — blood group, tissue typing and the antibodies that determine compatibility. It can conclude that transplantation is not appropriate, and that conclusion is reached honestly rather than by leaving someone on a list indefinitely.

Immunosuppression and kidney transplant rejection

Kidney transplant rejection is the immune system recognising the graft as foreign. It is far less common than it once was and it is usually treatable when caught — which is the whole reason for the monitoring schedule that follows a transplant.

The essential fact for any transplant recipient is that rejection is usually silent. It shows as a rising creatinine on a routine blood test before it produces any symptom at all, which is why blood tests are frequent early and continue for life, and why a transplant patient who feels perfectly well still attends. Where rejection is suspected, a biopsy of the graft establishes the type — cellular or antibody-mediated — because the treatments differ.

Immunosuppression is lifelong and is a balance rather than a target: too little and the graft is rejected, too much and infection and cancer risk rise. That balance is managed with drug level monitoring, and it carries obligations that must be understood before the operation rather than after — the medicines are taken at fixed times and never stopped or altered independently, infections are reported early rather than waited out, skin cancer surveillance and sun protection become permanent, and vaccination status is reviewed since live vaccines are generally not given afterwards. Every one of those decisions belongs to the transplant team.

Plasmapheresis and plasma exchange

Plasmapheresis separates plasma from the blood cells and removes it, replacing it with albumin or donor plasma. It exists to strip out something circulating in the plasma that is causing harm — usually an antibody — and it is a rescue rather than a routine treatment.

Its established indications in this specialty are specific: anti-GBM disease, in which an antibody attacks the glomerular basement membrane and lung, where speed determines whether the kidney is saved; severe ANCA-associated vasculitis in selected situations; antibody-mediated rejection of a transplant; desensitisation before an incompatible transplant; and the thrombotic microangiopathies, where it is the treatment for TTP specifically.

It works only alongside treatment that stops the antibody being produced — removing antibody without suppressing its production achieves a temporary fall and nothing more, which is why plasma exchange is always part of a regimen rather than a treatment on its own.

Haemolytic uraemic syndrome (hemolytic uremic syndrome) and uraemia (uremia)

Hemolytic uremic syndrome is the triad of destruction of red cells as they pass through damaged small vessels, a low platelet count, and acute kidney injury. The typical form in children follows infection with Shiga toxin-producing E. coli, usually after bloody diarrhoea, and most children recover kidney function with supportive care. The atypical form is driven by uncontrolled activation of the complement system, often with an underlying genetic predisposition, and it behaves entirely differently — it recurs, it damages kidneys permanently, and it is treated with complement-blocking therapy, which transformed its outlook.

Distinguishing the two, and distinguishing both from TTP, is urgent, because the treatments differ and delay costs kidney function. The features that separate them are the history, the trigger and specific laboratory testing.

Uremia is the syndrome produced by accumulated waste when the kidneys fail — nausea, loss of appetite, a metallic taste, itching, restless legs, disturbed sleep, poor concentration, and in advanced cases confusion and inflammation of the lining of the heart. It is what dialysis relieves, and its appearance is one of the clinical triggers for starting it.

Kidney infection and pyelonephritis

A kidney infection — pyelonephritis — is bacterial infection of the kidney itself rather than the bladder, and the distinction is worth understanding because the treatment and the seriousness differ. Bladder infection causes burning and frequency; a kidney infection adds fever, shivering, pain in the flank and often nausea, and someone with it is unwell in a way that cystitis does not produce.

Most cases are treated with antibiotics and recover fully. What changes the situation is obstruction: an infected kidney behind a blocked ureter is a surgical emergency, because antibiotics cannot sterilise urine that cannot drain, and the obstruction has to be relieved — that is a urology problem and is why imaging is done when a kidney infection does not settle promptly.

Its nephrological relevance is the long tail. Repeated infections, particularly with reflux in childhood, scar the kidney and produce reflux nephropathy — a cause of hypertension and chronic kidney disease that presents decades later in someone who remembers only that they had a lot of infections as a child. Antibiotic choice, duration and any prophylaxis are decided by the treating doctors, and recurrent infection in an adult is investigated for an underlying cause rather than treated repeatedly.

Your multidisciplinary team

The nephrologist establishes the stage and the cause, slows the decline, manages the complications and decides with the patient what happens when function runs out. The renal dietitian translates four separate dietary restrictions into food someone will actually eat, and adjusts them as the stage changes — this role prevents more harm than it is given credit for. The dialysis nurse delivers the treatment, trains home patients and manages access. The transplant coordinator runs the work-up, the waiting list and the follow-up. The renal pharmacist checks every prescription against kidney function, which in a population taking a dozen medicines is a substantial safety layer.

Around them: transplant surgery for the operation, vascular surgery for dialysis access, urology for obstruction, stones and the cystic lesions that need it, endocrinology for the diabetes that causes much of this, cardiology because cardiovascular disease is what most people with kidney failure actually die of, internal medicine for the systemic diseases behind glomerular disease, and nutrition and dietetics for the diet.

The international patient journey

Nephrology travels differently from surgery. There is rarely a single procedure to schedule; what a patient usually needs is a definitive assessment, a diagnosis where one has not been reached, and a plan that can be carried out at home.

Send the trend, not one result

The single most valuable thing in a nephrology file is a series of creatinine and eGFR results over time, because the slope determines the plan and one value determines almost nothing. With it: urine protein quantification, ultrasound reports, the full medication list including anything bought without prescription, and any previous biopsy report with its full description rather than the summary line.

Review before travel

The review establishes whether the question is diagnostic, whether a biopsy is likely to be needed, and what can be answered without travelling at all. A proportion of reviews conclude that the management already in place is correct and that a second opinion confirms rather than changes it — which is a legitimate outcome and is stated as readily as any other.

Assessment on arrival

Blood and urine work repeated in one laboratory so the results are comparable, imaging, and where indicated a kidney biopsy with the observation period that follows it. Dialysis patients travelling for assessment need their sessions arranged in advance as part of the booking rather than on arrival, and that is organised before travel.

A plan that works at home

What matters most in this specialty is that the plan survives the flight. That means a written regimen naming the medicines, the doses and the monitoring intervals; the blood tests to be done locally and the thresholds that should prompt contact; and, where transplantation or dialysis is being planned, a clear statement of what needs to happen and when. Immunosuppression after a transplant is managed by the transplant team indefinitely, and follow-up arrangements are made before departure rather than after.