Kidney failure refers to a decrease in the kidneys’ ability to filter blood and perform their various physiological functions. According to the HAS and the French Society of Nephrology, it is classified into two main clinical forms that differ in their progression.
Acute kidney injury (AKI) involves a sudden deterioration (over hours to days) in kidney function, which is often reversible if the cause is quickly identified and treated.Chronic kidney disease (CKD) is defined by a progressive and persistent (lasting more than three months) decline in glomerular filtration rate (GFR), progressing through stages of increasing severity. Essential kidney functions include: filtration of nitrogenous waste products (urea, creatinine), regulation of fluid volume, maintenance of electrolyte balance (sodium, potassium, calcium, phosphorus), regulation of acid-base balance, production of erythropoietin (which stimulates red blood cell formation), and activation of vitamin D. Impaired renal function accounts for the wide range of clinical manifestations seen in this complex condition.
Chronic kidney disease has several main causes identified by national and international nephrology guidelines. Understanding these causes guides prevention and treatment.
Diabetes (type 1 and, especially, type 2) is the leading cause of end-stage chronic kidney disease in France and in most developed countries. Diabetic nephropathy often progresses silently for several years before being detected.High blood pressure is the second leading cause: chronic hypertension gradually damages the renal blood vessels and accelerates the loss of function. Glomerulonephritis and other forms of chronic nephritis (damage to the filtration structures) are the third major cause. Polycystic kidney disease is a common genetic cause. Chronic urinary tract obstructions (recurrent stones, kidney stones, advanced prostatic hypertrophy, urological tumors) can lead to kidney failure by affecting the renal parenchyma. Certain nephrotoxic medications used over the long term (NSAIDs, lithium, cyclosporine, certain anticancer drugs) are also among the identifiable causes.
The diagnosis of kidney failure is based on a structured approach combining laboratory tests, imaging, and sometimes histology. It is initially managed by the primary care physician, with confirmation and treatment handled by a nephrologist.
The initial laboratory workup includes: serum creatinine with calculation of the estimated glomerular filtration rate (eGFR) using the CKD-EPI formula, which is central to the diagnosis; blood urea nitrogen; serum electrolyte panel (particularly serum potassium and bicarbonate levels to check for metabolic acidosis); a complete blood count (to check for associated anemia).Urinalysis includes a urine test strip, a urine culture if infection is suspected, and a proteinuria test using a single sample with a protein-to-creatinine ratio or a 24-hour urine collection, to detect proteinuria or microalbuminuria (an early marker of diabetic nephropathy). Renal and bladder ultrasoundimaging assesses kidney size, cortical-medullary differentiation, and checks for obstruction or dilation of the renal cavities. Depending on the case: non-contrast abdominal CT scan, MRI, renal artery Doppler. A renal biopsy, performed in a specialized setting under ultrasound guidance, may be necessary to determine the histological cause and guide treatment.
Chronic kidney disease often remains asymptomatic for a long time, which explains why it is frequently diagnosed late. Symptoms generally appear in advanced stages.
The most common clinical manifestations include: fatigue and generalized weakness related to anemia and the accumulation of uremic toxins; edema (swelling of the ankles, feet, and sometimes the face and eyelids) indicating fluid and sodium retention; changes in urine output (oliguria, sometimes initially polyuria) and in the appearance of the urine; nausea, vomiting, and loss of appetite in advanced stages; sleep disturbances, difficulty concentrating, and mental sluggishness; diffuse skin pruritus related to urea deposits and calcium-phosphorus imbalances; shortness of breath due to fluid overload or acidosis; muscle cramps and restless legs. In very advanced stages (uremia), neurological disorders (drowsiness, confusion), effusions (uremic pericarditis), and gastrointestinal bleeding may occur. Any suggestive symptom, particularly in at-risk individuals (those with diabetes, high blood pressure, or the elderly), warrants prompt medical consultation. The range of products designed for urinary comfort can help manage certain symptoms as a complement to medical care.
The treatment of kidney failure depends on the stage, cause, and overall clinical context. Management is necessarily multidisciplinary and coordinated by a nephrologist.
Etiological treatment is a priority: strict control of diabetes and blood pressure, treatment of inflammatory or autoimmune kidney diseases, and resolution of any urological obstructions. Nephroprotective treatments are central to management: renin-angiotensin system inhibitors (ACE inhibitors or ARBs) that reduce intraglomerular pressure and proteinuria; SGLT2 inhibitors (dapagliflozin, empagliflozin), which have demonstrated significant renal benefit in several recent studies; and nonsteroidal mineralocorticoid receptor antagonists (finerenone) in certain diabetic patients. Symptomatic treatments include: correction of anemia (recombinant erythropoietin, iron), maintenance of calcium-phosphorus balance (phosphate binders, active vitamin D derivatives), and correction of metabolic acidosis. In the end-stage, renal replacement therapies become necessary: hemodialysis (in a center or at home), home peritoneal dialysis, or kidney transplantation (from a living or deceased donor). Self-medication, particularly with NSAIDs, must be strictly avoided and discussed with the nephrologist.
Preventing kidney failure relies primarily on managing modifiable risk factors. Several simple measures have been shown to be effective, particularly in at-risk individuals.
Strict control of diabetes through blood glucose monitoring, adherence to treatment, and annual screening for microalbuminuria. Strict control of blood pressure (generally targeting less than 130/80 mmHg in individuals at risk for kidney disease) through regular monitoring and appropriate treatment.A balanced diet with sodium restriction (less than 6 g of salt per day), moderation in animal protein intake, and limiting ultra-processed foods.Adequate hydration (1.5 to 2 liters of water per day for an adult with no contraindications) to support kidney function.Avoiding self-medicationwith nephrotoxic drugs, particularly long-term use of NSAIDs; any chronic treatment should be discussed with a doctor. Maintaining a healthy body weight and limiting alcohol consumption.Quitting smoking, which exacerbates kidney disease and is an associated cardiovascular risk factor. Regular screening for at-risk individuals (those with diabetes, high blood pressure, a family history of kidney disease, those over 60, or those exposed to nephrotoxic substances): serum creatinine and albuminuria should be measured at least annually, according to HAS recommendations.
Chronic kidney disease and cardiovascular disease are closely linked through a complex system of interactions known as “cardiorenal syndrome.” This bidirectional relationship shapes the patient’s overall management.
Patients with chronic kidney disease have a significantly increased cardiovascular risk compared to the general population, at all stages of the disease. Several mechanisms explain this increased risk. Fluid and sodium retention and disruption of the renin-angiotensin system contribute to hypertension.The accumulation of uremic toxins and mineral and bone disorders (hyperphosphatemia, secondary hyperparathyroidism) accelerate vascular calcification and atherosclerosis.Anemia, which is common, increases the cardiac workload.Low-grade chronic inflammation and oxidative stress contribute to vascular damage. Cardiovascular mortality is elevated in patients with kidney failure, particularly those on dialysis. Cardiovascular prevention is therefore an integral part of nephrological care: control of blood pressure, diabetes, and LDL cholesterol; smoking cessation; appropriate physical activity; and, in some cases, antiplatelet therapy based on medical evaluation.
Diet plays a central role in the management of kidney disease. Dietary recommendations vary depending on the stage of the disease and must be tailored to the individual in consultation with a dietitian specializing in nephrology.
Several principles guide dietary adjustments. Sodium restriction (less than 6 g of salt per day, or even less) to control blood pressure and limit fluid retention. Adjustment of protein intake based on the stage of the disease: moderate restriction (0.6 to 0.8 g/kg/day) in moderate to severe kidney failure, while avoiding malnutrition. Sufficient energy intake to prevent muscle catabolism. Monitor potassium intake in advanced stages: limit dried fruit, bananas, chocolate, certain vegetables (spinach, Swiss chard, potatoes), and legumes based on lab results. Adjust phosphorus intake: limit dairy products, processed meats, and phosphate-rich sodas. Fluid intake should be adjusted according to urine output—neither too restrictive nor excessive. Limit ultra-processed foods and added sugars. In dialysis patients, protein intake should, on the contrary, be increased (1.1 to 1.2 g/kg/day) to compensate for losses. A specialized dietary consultation is invaluable for personalizing the diet.
Nephrology has seen significant advances in recent years. Several innovations are gradually transforming patient care and improving outcomes for patients.
SGLT2 inhibitors (dapagliflozin, empagliflozin) have marked a major turning point: initially developed for diabetes, they have demonstrated significant renal and cardiovascular benefits in several kidney diseases, including in non-diabetic patients with proteinuria. Nonsteroidal mineralocorticoid receptor antagonists (finerenone) offer a new treatment option for certain patients with diabetes. Targeted biologic therapies for autoimmune glomerulonephritis (rituximab, belimumab) improve prognosis. Dialysis techniques are evolving: new, more efficient machines; automated peritoneal dialysis at home; and home hemodialysis in certain centers. Kidney transplantation benefits from advances in immunosuppression, desensitization techniques for hyperimmunized patients, and donor exchange programs. Research on bioartificial organs, cell therapies, and xenotransplantation opens up longer-term prospects. Treatment protocols are defined in guidelines that are regularly updated by professional societies (French Society of Nephrology, KDIGO).
Chronic kidney disease can lead to several medical complications as the disease progresses. Regular screening for these complications and early management significantly improve quality of life and prognosis.
Anemia results from insufficient production oferythropoietin by the failing kidneys and leads to fatigue, exertional dyspnea, and a reduced quality of life. Its treatment relies on recombinant erythropoietin and iron supplementation. Mineral and bone disorders associated with chronic kidney disease (MBD-CKD) include hyperphosphatemia, hypocalcemia, active vitamin D deficiency, secondary hyperparathyroidism, osteodystrophy, and vascular calcifications. Fluid and sodium retention leads to peripheral edema, hypertension, and even acute pulmonary edema.Metabolic acidosis can exacerbate muscle catabolism and the progression of the disease. Cardiovascular disorders are numerous: hypertension, left ventricular hypertrophy, and uremic pericarditis in advanced stages. Protein-energy malnutrition is common, particularly in dialysis patients, and must be prevented. Infections are more common due to a certain degree of immunosuppression. Multidisciplinary care (involving a nephrologist, primary care physician, dietitian, and sometimes a cardiologist or endocrinologist) enables comprehensive management.
Several clinical signs should serve as warning signs and prompt a prompt medical consultation. Recognizing these warning signs allows for early intervention and improves the chances of preserving kidney function.
Warning signs that should not be ignored include: a noticeable decrease in urine output (persistentoliguria ) or a sudden change in urine output; cloudy, foamy, dark, or bloody urine; swelling of the ankles, legs, or eyelids, especially in the morning; unexplained fatigue and shortness of breath during exertion or at rest; persistent nausea and loss of appetite; widespread itching with no obvious dermatological cause; repeated muscle cramps, restless legs; unexplained sleep disturbances and difficulty concentrating; new-onset or difficult-to-control hypertension. In at-risk individuals (those with diabetes, high blood pressure, a family history of kidney disease, those over 60 years of age, or those exposed to nephrotoxic substances), annual screening for serum creatinine and albuminuria is recommended even in the absence of symptoms, according to the HAS. Any severe lower back pain, fever, or acute urinary symptoms should prompt a prompt medical evaluation, or even an emergency visit, depending on the circumstances.
