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Dialysis is a therapy that artificially removes wastes from the blood of patients whose kidneys can no longer perform this function adequately. There are two main types of dialysis: hemodialysis and peritoneal dialysis.
In hemodialysis, blood is filtered outside the body, in a dialysis machine. The patient’s blood is pumped to the machine, cleansed, then returned to the body. To prepare for regular hemodialysis treatments, a one-time minor surgery is performed to create a vascular access, which is essentially a large and strong vein, enough to sustain the high flow rate through the machine. This can be accomplished by fusing an artery to a vein, forming a so-called fistula; or by adding a synthetic tube – a graft. For emergency treatment, a catheter can be used for temporary access.
Once inside the machine, blood flows within tiny tubes surrounded by a dialysis solution, called dialysate. The walls of the tubes act as semipermeable membranes that allow only small molecules, such as water, nitrogenous wastes and electrolytes, to pass through. The filtration occurs by osmosis and diffusion, where water and solutes move from higher to lower concentration. The dialysis fluid contains solutes at the levels similar to those in healthy blood. Urea, potassium and other solutes that are present at higher levels in patient’s blood, move out to the dialysate, which is constantly replaced and discarded. At the same time, other substances can be added to the dialysis fluid to be administered to the patient. These may include: bicarbonate, to adjust the patient’s blood pH; erythropoietin, to compensate for its low production by the failing kidneys; and certain medications. Because of the increased risks of blood clotting associated with its contact with foreign surfaces, an anticoagulant such as heparin is usually added. The composition of dialysis fluid is typically prescribed by a nephrologist based on the patient’s needs.
Hemodialysis is normally performed as 4-hour treatments, 3 times a week, in a dialysis center. Complications include risks of blood infection, thrombosis, and internal bleeding due to the added anticoagulant.
In peritoneal dialysis, the dialysis fluid is introduced into the patient’s abdominal cavity via a catheter. The lining of the abdomen, the peritoneum, serves as the natural filtering membrane. The fluid remains in the body for several hours, allowing exchange and equilibrium with the blood running in the underlying vessels, before being discarded. The therapy can also be done automatically at night during sleep.
Peritoneal dialysis is less effective than hemodialysis, but because it can be performed for longer periods of time, the result is comparable. Peritoneal dialysis offers more flexibility, is better tolerated by patients, and less expensive, but is more often complicated with abdominal infections.

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Chronic kidney disease, CKD, is a gradual loss of renal function, typically developing over the course of months or years. Many conditions, both within and outside the kidneys, can cause progressive damage to the kidneys over time, leading to CKD. Of these, most common are diabetes and hypertension, both of which directly damage blood vessels within the kidney, destroying renal tissue. An acute kidney injury, if not completely resolved, may also become chronic kidney disease.
The severity of renal disease is evaluated based on glomerular filtration rate, GFR, an indicator of how well the blood is filtered by the kidneys. GFR is calculated as a function of serum creatinine, a waste product that accumulates in blood plasma when renal function declines. The calculation takes into account the patient’s age, gender and race.
Symptoms develop slowly over time, progressing from renal insufficiency to end-stage renal failure. Often, initial loss of renal tissue does not produce any symptoms, because the remaining healthy tissue becomes more active and can temporarily compensate for the loss, a phenomenon known as renal adaptation. Symptoms appear when a significant portion of kidney function is already lost. The ability to concentrate urine is usually the first to be impaired, resulting in frequent trips to the bathroom, especially at night. Other early signs include fatigue, loss of appetite, and decreased mental ability.
Because the kidneys remove metabolic wastes, control blood pH and fluid/electrolyte balance, as well as produce several hormones, loss of kidney function may result in a number of complications:
– Accumulation of toxic nitrogenous wastes can cause a range of symptoms, from nausea, vomiting to confusion and seizures.
– Reduced excretion of hydrogen ions leads to increased blood acidity, or metabolic acidosis.
– Reduced excretion of potassium results in potassium overload in the blood, or hyperkalemia, which may cause cardiac arrhythmias. Hyperkalemia usually occurs only in advanced stage, but excessive potassium intake or use of drugs that prevent potassium excretion, may precipitate the condition in earlier stages.
– Decreased excretion of phosphate results in hyperphosphatemia.
– Reduced renal production of calcitriol, an active form of vitamin D, contributes to low blood calcium level, or hypocalcemia. Low blood calcium stimulates production of parathyroid hormone, PTH, by the parathyroid gland. PTH promotes calcium release from bones in an attempt to raise blood calcium. This sequence eventually leads to an overactive parathyroid gland, or secondary hyperparathyroidism, which can develop before hypocalcemia occurs. As the bones continuously lose calcium to the blood, they become thin and weakened, a condition known as renal osteodystrophy. Symptoms include bone and joint pain, and increased risks of fractures.
– Reduced renal secretion of erythropoietin, a stimulating factor for red blood cell formation, can lead to anemia.
Diagnosis is based on renal function tests, which include blood and urine analysis. Ultrasound is performed to detect renal obstruction. It may also help in distinguishing chronic kidney disease from acute kidney injury based on kidney size.
Treatments aim to control the underlying condition, address the complications, and involve certain nutrition supplements and restrictions. End-stage kidney disease requires dialysis or kidney transplantation.

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Acute kidney injury, AKI, also known as acute renal failure, is a sudden, rapid loss of kidney function, typically within days or weeks.
The function of the kidneys is to filter blood plasma, removing metabolic wastes in urine, while also adjusting urine composition to maintain balance of various blood parameters. In AKI, metabolic wastes accumulate; and fluid, electrolyte and acid-base disorders may develop quickly. Of the many possible complications, most serious are potassium overload – hyperkalemia, and excess of fluid volume, or hypervolemia. Usually, both kidneys must fail for AKI to be diagnosed.
While AKI can be caused by a rapidly progressing intrinsic kidney disease, it is most commonly a consequence of an underlying condition outside the kidney.
Causes are classified as prerenal, renal and postrenal, with prerenal being most common.
Urine formation occurs in the functional units of kidneys, called the nephrons. Blood enters the nephrons via the afferent arteriole, passes through a ball of capillaries called the glomerulus, where filtration takes place, then leaves via the efferent arteriole. Blood pressure inside the glomerulus must be high enough to enable filtration. This is achieved by having the afferent arteriole significantly larger than the efferent arteriole, creating a blood flow with a large inlet and small outlet.
Prerenal AKI is usually due to an inadequate blood flow to the kidneys. Major causes include extracellular fluid volume depletion and decreased blood pressure, both of which reduce the glomerular filtration rate. Normally, autoregulatory mechanisms within the kidney, which dilate the afferent arteriole in response to volume loss, can compensate for a certain degree of low blood flow. AKI develops when hypoperfusion is severe, or when these mechanisms are compromised in patients with preexisting chronic kidney disease. Medications that cause dilation of the efferent arteriole or constriction of the afferent arteriole, reduce the pressure inside the glomerulus, and may contribute to development of AKI.
In patients with prerenal AKI but otherwise healthy kidneys, renal function typically returns to normal after the underlying condition is resolved, or the offending drug is discontinued.
Renal causes refer to intrinsic problems within the kidney, such as inflammation or necrosis of any of its components: the glomeruli, renal tubules, and interstitium.
Postrenal causes include various types of obstruction in the storage or voiding parts of the urinary system. These range from microscopic obstruction within renal tubules, to blockage of ureters by kidney stones, to urethral obstruction due to enlarged prostate in men.
Some AKI may involve problems at MORE than one level. For example, renal hypoperfusion, a prerenal cause, may sometimes be severe enough to induce ischemia of renal tubule cells, leading to intrinsic kidney disease. As the cells die, cellular debris may clog the tubules, becoming a postrenal cause.
Initially, symptoms of AKI are commonly masked by those of the underlying condition. In a later stage, symptoms are due to accumulation of nitrogenous wastes and disturbances of fluid and electrolyte balance. Urine output may or may not be reduced.
Diagnosis is based on renal function tests, such as serum creatinine and urea, serum electrolytes, urinary sediment, urine output and urinalysis.
Cause must be determined. Prerenal causes are usually apparent. Ultrasound is commonly performed to detect postrenal blockage.
Treatments aim to address the underlying cause, although some patients may also require fluid and electrolyte management, or dialysis.

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The urinary system is best known for removing metabolic wastes from the body in the form of urine, but its importance goes far beyond that function. As the kidneys filter large amounts of blood plasma, they are well positioned to detect changes in blood volume and composition, and respond accordingly. In fact, the kidneys are critical in maintaining steady state, or homeostasis, of many blood parameters, including blood volume and pressure, osmolality, concentrations of various solutes, blood pH, and red blood cell count.
Urine formation occurs in functional units of the kidneys called the nephrons. A nephron consists of two major parts: a glomerular capsule, or Bowman’s capsule; and a long renal tubule. Renal tubules of several nephrons connect to a common collecting duct. Basically, blood plasma is first filtered in the Bowman’s capsule. The filtrate then moves through the long winding renal tubule, alongside a network of blood capillaries, before draining into the collecting duct. This long passage is where the blood reabsorbs what is needed, and additional wastes are removed. This process determines the composition of urine and is regulated accordingly to the body’s needs.
The kidneys control blood volume and blood pressure by removing more or less water as necessary. Water excretion by the kidneys is regulated by a number of hormones, including:
– Vasopressin, also known as antidiuretic hormone, a hypothalamic hormone released in response to low blood volume or high plasma osmolality. Vasopressin causes the kidneys to retain more water by increasing water permeability of the collecting duct.
– Aldosterone, the “salt-retaining hormone”, secreted by the adrenal cortex in response to low blood sodium. Aldosterone acts on the distal tubule and collecting duct to increase reabsorption of sodium, which is followed by increased retention of water.
– The kidneys themselves produce an enzyme called renin in response to low blood pressure. Renin initiates a two-step process that produces the hormone angiotensin II. Angiotensin II increases blood pressure in several ways. It constricts blood vessels, promotes the release of vasopressin and aldosterone, and stimulates thirst centers in the brain to encourage water intake.
– Atrial natriuretic peptide, ANP, secreted by the atrial myocardium of the heart, in response to high blood pressure. ANP reduces blood pressure in a number of ways. It directly dilates blood vessels. It increases glomerular filtration rate, thereby removing more fluid in urine. ANP inhibits the secretion of renin, and subsequently aldosterone. ANP also inhibits sodium reabsorption by the collecting duct.
The kidneys control blood pH by adjusting the amount of excreted ACIDS and reabsorbed bicarbonate. Plasma bicarbonate is filtered in the glomerulus during the first step of urine formation, then reabsorbed back into the blood in the proximal tubule. The amount of reabsorbed bicarbonate is regulated in response to changes in blood pH. It increases during acid loads and decreases during alkali loads. In addition, the collecting duct also generates new bicarbonate which exits into the blood during high acid loads.
The kidneys secrete erythropoietin, EPO, a stimulating factor for red blood cells formation. Low levels of EPO are constantly produced to compensate for normal blood cell turnover. When red blood cell count drops, such as during blood loss, the resulting oxygen-deficiency state is detected by the kidneys, which respond by increasing their EPO secretion.
The kidneys are also involved in calcium homeostasis. In response to low blood calcium levels, parathyroid hormone, PTH, stimulates the kidneys to produce the hormone calcitriol. Calcitriol promotes absorption of dietary calcium in the small intestine and increases calcium reabsorption by the kidney. PTH itself also causes the kidneys to retain calcium.

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The kidneys filter blood plasma, removing metabolic wastes, toxins from the body and excrete them in the form of urine. During this process, they also maintain constant volume and composition of the blood, or homeostasis.
Blood enters the kidney via the renal artery, which divides to smaller arteries and finally arterioles. The arterioles get into contact with functional units of the kidney called nephrons. This is where blood filtration and urine formation take place. The filtered blood is then collected in to a series of larger veins and exits the kidney through the renal vein. The urine is collected in collecting ducts and leaves the kidney via the ureters.
Each kidney contains over a million nephrons. A nephron consists of 2 major parts: a capsule known as glomerular capsule, or Bowman’s capsule; and a long renal tubule. Renal tubules of several nephrons connect to a common collecting duct.
There are 3 steps in the formation of urine:
– glomerular filtration takes place in the Bowman’s capsule
– tubular re-absorption and secretion occur in the renal tubule
– water conservation happens in the collecting duct
Blood enters the Bowman’s capsule via the afferent arteriole, passes through a ball of capillaries called the glomerulus, and leaves via the efferent arteriole. The afferent arteriole is significantly larger than the efferent arteriole, creating a blood flow with a large inlet and small outlet. As a result, the blood hydrostatic pressure in these capillaries is much higher than normal. Hydrostatic and osmotic pressures drive water and solutes from blood plasma through a filtration membrane into the capsular space of nephron. The filtration membrane acts like a sieve allowing only small molecules to pass through. These include water, inorganic ions, glucose, amino acids and various metabolic wastes such as urea and creatinine. This fluid is called glomerular filtrate. The amount of filtrate produced per minute is called glomerular filtration rate, or GFR. The GFR is kept at a stable value by several feedback mechanisms within the kidneys. This is known as renal autoregulation. The GFR is also under sympathetic and hormonal control. GFR control is generally achieved by constriction or dilation of the afferent arteriole, which causes the glomerular blood pressure to fall or rise, respectively.
In a healthy person, the total filtrate volume amounts between 150 and 180 litters a day. However, only about 1% of this is excreted as urine, the rest 99% is re-absorbed back to the blood as the filtrate flows through the long renal tubule. This is possible because the efferent arteriole, after exiting the Bowman’s capsule, branches out to form a network of capillaries, known as peri-tubular capillaries, which surround the renal tubule.
The first part of the renal tubule – the proximal convoluted tubule, re-absorbs about two thirds of the filtrate. In this process, water and solutes are driven through the epithelial cells that line the tubule into the extracellular space. They are then taken up by the peritubular capillaries. Sodium re-absorption is most important, as it creates osmotic pressure that drives water and electrical gradient that drives negatively charged ions. Sodium level inside the epithelial cells is kept low thanks to the sodium-potassium pumps that constantly pump sodium ions out into the extracellular space. This creates a concentration gradient that favors sodium diffusion from tubular fluid into the cells. Sodium is absorbed by symport proteins that also bind glucose and some other solutes. Nearly all glucose and amino acids are re-absorbed back to the blood at this stage. About half of nitrogenous wastes also re-absorbs back to the bloodstream. The kidneys reduce the blood levels of metabolic wastes to a safe amount, but do not completely eliminate them. Some of the re-absorption also occurs by the paracellular route through tight junctions between the epithelial cells.
At the same time, tubular secretion, where additional wastes, drugs and other solutes leave the bloodstream to join the tubular fluid, also takes place.
The processes of re-absorption and secretion continue in the nephron loop – the loop of Henle, and the distal convoluted tubule. However, these parts of the tubule also have some other important functions.
The main function of the loop of Henle is to create and maintain an osmolarity gradient in the medulla that enables the collecting ducts to concentrate urine at a later stage. The ascending limb of the loop actively pumps sodium out making the medulla “salty”. The descending limp of the loop is permeable to water but much less to sodium. As the water exits the tubule by osmosis, the filtrate gets more and more concentrated as it reaches the bottom. The ascending limb, on the other hand, is permeable to ions but not water. As a result, the filtrate loses sodium as it goes up and becomes more diluted at the top of the loop. The medulla is in equilibrium with the loop and hence has the same salinity gradient – saltier at the bottom.
Re-absorption and secretion in the distal convoluted tubule are under control of various hormones. This is how the kidney respond to the body’s needs and adjust the composition of urine accordingly.
The collecting duct receives tubular fluid from several nephrons. The main function of the collecting duct is to concentrate urine and therefore conserve water. This is made possible by the osmolarity gradient generated by the loop of Henle. As it gets saltier deep in the medulla, the filtrate loses more and more water as it flows down the collecting duct. The collecting duct is also under hormonal control so it can adjust the amount of re-absorbed water accordingly to the body’s state of hydration. For example, when the body is dehydrated, more water is re-absorbed back to the blood and the small volume of excreted urine is more concentrated.

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A infecção do trato urinário, ou ITU, é uma infecção em qualquer parte do sistema urinário – os rins, ureteres, bexiga e uretra.
Uma infecção da uretra, ou uretrite, pode causar sensação de queimação ao urinar e corrimento esbranquiçado. A infecção da bexiga, ou cistite, pode resultar em dor pélvica, aumento da frequência urinária, dor ao urinar e sangue na urina. Uma infecção renal, ou pielonefrite aguda, podem causar dor nas costas (possivelmente apenas em um lado), febre alta, calafrios e náuseas.
ITUs ocorrem tipicamente quando a bactéria entra no trato urinário através da uretra e multiplica-se na bexiga. Mais comumente, essas bactérias vêm a partir do trato digestivo, através das fezes. ITUs são mais comuns em mulheres devido à sua anatomia. Especificamente, a curta distância do ânus para a abertura da uretra e da bexiga, tornando mais fácil para as bactérias atingirem o sistema urinário a partir do trato digestivo. É por isso que a maioria das ITUs ocorrem, principalmente, em mulheres e afetam a bexiga e a uretra.
Outras bactérias podem ser trazidas com o contato sexual. As mulheres que usam certos tipos de controle de natalidade, como diafragmas ou agentes espermicidas, apresentam maior risco. A deficiência hormonal, durante a menopausa, também torna as mulheres mais vulneráveis à infecção.
Infecção apenas na bexiga pode ser facilmente tratada com antibióticos. No entanto, se não for tratada, uma infecção do trato urinário inferior podem espalhar-se para os rins, tornando-se mais perigosa. Uma infecção renal pode resultar em danos permanentes nos rins. Em casos raros, a infecção também pode se espalhar para a corrente sanguínea, podendo ser fatal.
Infecções do trato urinário podem ser evitadas seguindo os seguintes passos:
• Beber bastante líquidos – pois, aumentará a frequência urinária para expulsar as bactérias.
• Limpar da frente para trás depois de uma evacuação – isso ajuda a impedir que as bactérias nas fezes se espalhem para a uretra.
• Esvaziar a bexiga logo após a relação sexual para expulsar as bactérias.
• Evitar produtos femininos que podem irritar a uretra, como duchas e pós.
• Evitar diafragmas e espermicidas como métodos de controle de natalidade.

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A urinary tract infection, or UTI, is an infection in any part of the urinary system — the kidneys, ureters, bladder and urethra.

Symtomps:

An infection of the urethra, or urethritis, may cause burning sensation when urinating and cloudy discharge. A bladder infection, or cystitis, may result in pelvic pain, frequent, painful urination, and blood in urine. A kidney infection, or acute pyelonephritis, may cause back pain (possibly only on one side), high fever, chills and nausea.

Causes and Risk Factors:

UTIs typically occur when bacteria enter the urinary tract through the urethra and multiply in the bladder. Most commonly, these bacteria come from the digestive tract through fecal matter. UTIs are more common in women because of their anatomy. Specifically, the short distance from the anus to the opening of the urethra and bladder makes it easier for the bacteria from the digestive tract to reach the urinary system. This is why the most common UTIs occur mainly in women and affect the bladder and urethra.
Other bacteria may be brought over with sexual contact. Women who use certain types of birth control such as diaphragms or spermicidal agents are more at risk. Hormonal deficiency during menopause also makes women more vulnerable to infection.

Treatment and Complications:

Infection limited to the bladder can be easily treated with antibiotics. However, if left untreated, a lower urinary tract infection may spread up to the kidneys where it becomes more dangerous. A kidney infection may result in permanent kidney damage. In rare cases, an infection may also spread to the bloodstream and can be life threatening.

Prevention:

Urinary tract infections can be prevented following these steps:
– Drink plenty of fluids – to flush out bacteria more frequently.
– Wipe from front to back after a bowel movement – this helps prevent bacteria in stools from spreading to the urethra.
– Empty the bladder soon after intercourse to flush bacteria.
– Avoid feminine products such as douches and powders, which could irritate the urethra.
– Avoid diaphragms and spermicides as birth control methods

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La próstata es una glándula exocrina del tamaño de una nuez del sistema reproductor masculino. Está localizada justo debajo de la vejiga urinaria donde se envuelve alrededor de la primera parte de la uretra masculina. La glándula prostática produce un fluido lechoso que es expulsado dentro de la uretra para mezclarse con los espermatozoides durante la eyaculación. El fluido sirve como lubricante y nutrimento para los espermatozoides.
La hiperplasia prostática benigna, HPB, también llamada hipertrofia prostática benigna o agrandamiento de la próstata, es una condición en la que el tamaño de la glándula prostática está incrementado. Es considerada “benigna” porque no es un cáncer, y no incrementa el riesgo de cáncer. Sin embargo, cuando se hace suficientemente grande, el tejido prostático puede comprimir la uretra y bloquear el flujo de orina causando una serie de problemas de micción e infección del tracto urinario.
La HPB es muy común en hombres a medida que envejecen: aproximadamente el 50% de los hombres presentan cierto grado de HPB a la edad cercana a los 60 años, donde la mitad de ellos demuestran síntomas clínicos significativos. La HPB es un resultado de los cambios hormonales y es considerada una parte normal del envejecimiento masculino. En el tejido prostático que está envejeciendo, la tasa de proliferación celular inducido por las hormonas masculinas de alguna forma excede la tasa de la muerte celular programada o apoptosis. Esto resulta en un aumento en el número de células y el agrandamiento de la próstata.
Hay dos clases principales de medicamentos para el tratamiento de la HPB:
– bloqueadores alfa: estos fármacos relajan el músculo liso de la próstata y del cuello de la vejiga, aliviando así la obstrucción del flujo de orina.
– inhibidores de la 5-alfa reductasa: estos inhiben la producción local de dihidrotestosterona o DHT- la hormona responsable del agrandamiento de la próstata.
Para aquellos que no responden a la medicación, hay tratamientos mínimamente invasivos disponibles. Estas terapias no quirúrgicas usan calor para causar la muerte celular o necrosis en el tejido prostático. El calor es suministrado en pequeña cantidad y a una zona específica para minimizar el daño no deseado. Diferentes procedimientos difieren principalmente en el tipo de energía utilizada.
La resección transuretral de la próstata es un procedimiento quirúrgico para remover el tejido prostático a través de la uretra. Este procedimiento ha estado disponible durante mucho tiempo y todavía es considerado estándar de oro para el tratamiento de HPB severa. En la actualidad, generalmente se realiza cuando los medicamentos y métodos menos invasivos fallan.