The urinary system consists of two kidneys, which produce urine; two ureters, which carry urine to the urinary bladder, where it is temporarily stored; and the urethra, which transports urine to the outside of the body.

An adult typically has two kidneys, which are reddish-brown and bean-shaped (Image 1). Although their size can vary, the length of the average kidney is about 11 cm, the thickness about 2.5 cm, and the width is about 5 cm. The average weight of a single kidney is 15 g. The kidney's lateral border is convex, whereas the medial border is concave and indented in a depression called the renal hilus. All related structures enter or leave the kidney at the hilus [2,3].

There are essentially three general regions of each kidney: the cortex, the medulla, and the pelvis. These structures are located inside the renal capsule. Two of them—the cortex and the medulla—are often referred to collectively as the renal parenchyma. The cortex is directly beneath the renal capsule. This highly vascularized area of tissue is very sensitive to changes in blood flow. The medulla, located deep in the cortex, consists of 8 to 18 triangular renal pyramids. The renal pyramids are composed of collecting ducts that drain urine into the calyces. The cortex covers the base of the pyramids, and the tips (or papillae) project toward the renal pelvis. Cortical tissue known as renal columns dips into the medulla to separate the pyramids, and blood vessels that supply the cortex and medulla pass through these columns. Urine flows from the papillae into a minor calyx, and several of the funnel-shaped minor calyces emerge to form a major calyx. The major calyces join to form the renal pelvis, which is the expanded upper end of the ureter. At times, a catheter is positioned in the renal pelvis and must be irrigated with 4–6 mL of fluid (as ordered) to maintain catheter patency [7].

The nephron (Image 3) is the functional unit of the kidney and is primarily responsible for most of the mechanisms that provide internal homeostasis. Each kidney contains approximately 1.25 million nephrons, and each nephron in turn is composed of a vascular and tubular system that allows for the formation of urine. The nephrons are located in the renal parenchyma. Most nephrons are in the cortex (referred to as cortical nephrons), but juxtamedullary nephrons begin in the cortex and extend deep into the medulla [7].

Urine drips from the collecting tubules into the minor calyces and then the major calyces which, in turn, join the renal pelvis. From the renal pelvis, ureters transport urine to the urinary bladder. Each kidney typically has a single ureter responsible for emptying the urine formed by that kidney. Although the ureter's size varies, an average ureter is around 30 cm (almost 1 foot) long. The ureter's diameter ranges from 2–8 mm at various points in its structure. The ureters descend between the parietal peritoneum and the abdominal wall to the pelvic cavity, where they enter the bladder on its posterior inferior surface. Before opening into the bladder, the ureters travel obliquely through the bladder wall. As a result, pressure in the bladder can compress the ureters and help prevent urine from flowing back into the ureters, especially during bladder emptying [9].

The basic function of the nephron is to cleanse the blood of unwanted substances as it passes through the kidney. This results in the formation of urine and is accomplished through three specific processes that occur in the nephron: glomerular filtration, tubular reabsorption, and tubular secretion. Each process occurs dynamically in the kidneys' continuous efforts to maintain internal equilibrium [10].

As long as the various mechanisms that regulate renal blood flow maintain adequate hydrostatic pressure, glomerular filtrate will form. However, forces that oppose the formation of glomerular filtrate—plasma oncotic pressure and tubular filtrate pressure—must be overcome. Understanding plasma oncotic pressure is essential to appreciating the shift of body fluids and the formation of edema. Plasma oncotic pressure (also known as colloid osmotic pressure) is the pulling force of the proteins in the plasma that attempts to hold water in the vascular space and prevent its movement into the surrounding tissue. In the kidney, the plasma oncotic pressure attempts to keep water from being pushed onto the Bowman capsule. The typical glomerular filtration rate (GFR) is 130 mL/min/1.73 m². Thus, roughly 187,000 mL of glomerular filtrate is formed in 24 hours. For all practical purposes, glomerular filtrate is the same as plasma except it has no significant amount of plasma proteins. If all the components found in glomerular filtrate were excreted in the urine, death would occur. Therefore, much of the filtrate is returned to the blood via tubular reabsorption [11,12].

The kidneys regulate blood pressure through the maintenance of fluid volume and the release of the hormone renin, which stimulates powerful vasoconstrictive responses. Fluid volume in the extracellular compartment, and specifically the plasma, is controlled by the kidneys' ability to concentrate or dilute urine in response to serum osmolality. Thus, hypertonic plasma stimulates the release of ADH, the reabsorption of water, the expansion of intravascular volume, the decrease of urine output, and the elevation of blood pressure. This primary mechanism of volume expansion is partially responsible for the regulation of blood pressure [15,16].

Enlargement of one or both kidneys is most commonly related to the invasion and multiplication of neoplastic cells. If a mass becomes very large, it can put pressure on abdominal nerves or displace other abdominal organs and cause discomfort or pain [1,15].

As discussed, the kidneys maintain the normal osmolality of body fluids and, in conjunction with various endocrine mechanisms, control the appropriate balance of electrolytes in body fluids. Excesses and deficits of various electrolytes result in serious problems in the maintenance of normal nerve transmission and muscle conduction. Sodium, potassium, calcium, and magnesium are the major cations under the regulation of the kidneys. Some major anions (e.g., chloride, bicarbonate), as well as other anions such as sulfates, phosphates, and proteinate, are also under direction by the renal system [21,22].

The kidneys are responsible for excreting the acids produced by the metabolism of amino acids. The excretion of hydrogen ions by the kidneys is accomplished by the conservation of bicarbonate, the secretion of ammonia, and the excretion of hydrogen in exchange for sodium. The kidneys work with blood buffers and the pulmonary system to maintain a normal blood pH of 7.35–7.45. Blood buffers maintain this narrow range of acceptability; they almost instantaneously convert acids for either pulmonary excretion as carbon dioxide or for renal excretion through the conservation of bicarbonate or the exchange of sodium or potassium for hydrogen [23,24].

Azotemia is the accumulation of uremic toxins (urea, uric acid, and creatinine) in the blood. Uremia refers to azotemia with clinical symptoms. The accumulation of uremic toxins can result in neurologic complications, gastrointestinal bleeding, and skin changes resulting from urochrome pigments deposited in the skin. This pigmentation, combined with anemia, results in the pale yellow-gray skin color characteristic of patients with renal failure. Pruritus, also common, is thought to be the result of a buildup of the urochrome pigments in the skin as well as the crust of urate crystals that accumulates on the skin (called uremic frost). Increased parathyroid hormone production is also a possible cause of pruritus [14,18].

Uremic pericarditis is fairly common for patients with ESRD. Although this condition usually develops within 12 months of the initiation of dialysis, a later onset has also been observed. This inflammatory response is believed to be related to nitrogenous waste products not removed by dialysis. Fluid accumulates within the pericardial sac (pericardial effusion). With increased membrane irritability and platelet aggregation problems, the effusion may be serosanguineous. Massive pericardial effusions (greater than 2,000 mL) may accumulate over a period of days to weeks, seriously altering cardiovascular hemodynamics. Cardiac tamponade (compression of the heart from excessive fluid in the pericardial sac) will result in death unless medical intervention, surgical intervention, or both relieve the fluid accumulation [1,26].

The neurologic manifestations of uremia include uremic encephalopathy and peripheral neuropathy associated with azotemia and metabolic acidosis. Uremic encephalopathy (characterized by altered mentation/intellectual processes, tremors, and myoclonus) is associated with the onset of uremic manifestations. Asterixis (a flapping tremor of the hands) is an early manifestation caused by increased irritability of the central nervous system from elevated serum ammonia levels. This symptom is important, because tonic-clonic seizures may develop if the encephalopathic process is not corrected [1,26].

In general, platelet dysfunction is usually a problem with platelet aggregation—the platelet count is normal, and there is no alteration in the ability to produce platelets. In the uremic environment, however, the platelets do not promote the clotting mechanism as well. The results of other clotting tests (prothrombin time and partial thromboplastin time) are normal, but bleeding time may be prolonged. Impaired platelet function in the uremic environment is believed to be responsible for the frequent and easily induced bleeding into the skin and mucous membranes of the patient with either acute or chronic renal failure. Mucous membrane irritation, particularly of the gastrointestinal tract, along with the frequent presence of occult blood, indicates that a uremic environment persists despite dialysis therapy [1,26].

Among medications that may have a toxic effect on the kidneys, are a number of common antibiotics (e.g., penicillin, neomycin, kanamycin, amphotericin). Probably the most nephrotoxic category of antibiotics is the aminoglycosides (e.g., gentamicin, vancomycin, tobramycin). Other nephrotoxic drugs include sulfonamides, salicylates, thiazides, and furosemide [29,30].

Changes in the urine's appearance may be the presenting problem. Hematuria can be a serious sign, as it may be indicative of cancer. However, it also may be related to anticoagulant therapy, excessive exercise, infection, or trauma. If the urine is excessively alkaline, patients may describe it as being bright red or coffee-colored. If the urine is excessively acidic, blood can give the urine a cloudy or smoky appearance. In most cases, however, cloudy urine is the result of pus in the urine (pyuria). In severe pyuria, urine is also malodorous. Almost colorless urine usually results from excessive fluid intake, chronic renal disease, diabetes insipidus, or diabetes mellitus. Dark yellow-orange urine suggests dehydration or ingestion of medications or foods that discolor the urine. It is important to know when the change in urine color began and if it is constant, intermittent, or triggered by specific events [27,28]. Certain medications, such as phenazopyridine, can cause discoloration of the urine. It is important for history-taking to include any medications taken prior to urine testing. While dyes in medications can interfere with urine dip testing, they should not interfere with urine microscopy or urine culture [133].

Stress incontinence is a common problem for women. As noted, weakness can develop in the bladder-urethral sphincter mechanism through the stretching of pelvic muscles during childbirth or the pressure of the uterus on the bladder during pregnancy. In the elderly, relaxation of pelvic musculature also contributes to the incontinence. Frequent catheterizations and the use of forceps during delivery increase the chances for development of stress incontinence. When questioned, women may state that they need to wear sanitary pads or incontinence briefs [27].

Nurses should also determine if the patient maintains an adequate fluid intake (1,500–2,000 mL per day). If the patient has an excessive intake of milk and vitamin D, this could lead to hypercalciuria. Proteinuria, hematuria, or both can be a normal finding in people who exercise excessively. Immobility because of disability, fracture, thrombophlebitis, or surgery can predispose patients to the development of renal calculi [25,35].

Family history of congenital disorders should also be determined, including polycystic kidney disease and congenital malformations of the urinary tract. A strong family history of diseases such as diabetes or hypertension is also significant because these diseases tend to cause renal problems [37].

Serum creatinine measurements primarily reflect the ability of the kidneys to excrete creatinine—the waste product of the breakdown of phosphocreatine during skeletal muscle metabolism. The normal serum creatinine level is 0.6–1.5 mg/dL, but it varies with sex and individual muscle mass characteristics. Serial changes in serum creatinine levels are significant in evaluating and interpreting renal function, because this substance is excreted entirely by the kidneys and is therefore directly proportional to excretory function. Serum creatinine levels are less affected by factors such as dehydration, malnutrition, or hepatic function than BUN levels. Therefore, serum creatinine levels are more accurate than BUN levels in assessing renal function [38].

The best test to measure overall renal function is the creatinine clearance test, a mathematical calculation that compares the amount of creatinine filtered in a 24-hour urine collection with the amount of creatinine that remains in the serum. Because almost all creatinine is excreted and other variables do not influence muscle metabolism and renal excretion, creatinine clearance is regarded as the best indicator of renal function. Although a 24-hour collection is preferred, a 12-hour or shorter collection may be acceptable in some situations [38].

Specific gravity, a measure of the concentration of particles in the urine, reflects the ability of the kidney tubules to concentrate or dilute urine. The normal specific gravity is 1.016–1.022, but it can range from 1.001–1.040. The specific gravity increases in patients with:

In contrast, urine specific gravity decreases in patients with:

Percutaneous nephrostomy (PCN) provides a less invasive means to drain the renal collecting system in cases where obstruction of the kidney and ureter has resulted in hydronephrosis. Most often used for patients with kidney stones or bladder or pelvic tumor obstructions, PCN may be used to divert urine from the renal collecting system to allow leaks and fistulas to heal. The procedure is often performed after attempts at placing a ureteral stent through retrograde cystoscopy have proven unsuccessful. Providing drainage for that kidney is an urgent necessity, and PCN provides an exact method of accomplishing this task [39].

Indications for retrograde pyelogram include the evaluation of congenital ureteral obstruction, evaluation of acquired ureteral obstruction, elucidation of filling defects and deformities of the ureters or intrarenal collecting systems, opacification or distention of the collecting system to facilitate percutaneous access (in conjunction with ureteroscopy or stent placement), evaluation of hematuria, surveillance of transitional cell carcinoma, and evaluation of traumatic or iatrogenic injury to the ureter or collecting system.

Patients are positioned prone for kidney biopsies. Specimens are collected by means of long sampling needles. The procedure is usually safe, but some caveats apply, as in sampling for lupus [41]. Some referring physicians prefer to admit their patients for overnight observation, to closely monitor for excessive bleeding.

Mild or severe generalized itching accompanies ESRD and the development of uremia. The production and elimination of urate crystals by the skin and the increased production of parathyroid hormone are believed to be the causes of intense pruritus. Dry skin or perspiration and other moisture can worsen the pruritus [33,34].

In patients with ESRD and uremia, pruritus is often not relieved with the initiation of dialysis. Interventions that may provide comfort include avoiding agents known to dry the skin (e.g., soaps, lotions that contain alcohol). Bathing without soap will remove the uremic frost that compounds itching; bath water will be yellow from the urochrome pigments. Oil-based lotions and soaps containing lanolin or a high fat content should be encouraged. In addition, patients may be prescribed phosphate-binding agents; control of the phosphorous-calcium balance will moderate the production of parathyroid hormone [27,28]. Keeping the patient's fingernails short can help avoid lacerations and related infections.

Patients who are losing excessive protein (e.g., patients with proteinuria secondary to nephritic syndrome, patients on peritoneal dialysis) require a high-protein diet (1.2–1.3 g/kg body weight/day). In contrast, patients with ESRD who are becoming uremic or are undergoing chronic hemodialysis generally require a protein-restricted diet (0.6–0.8 g/kg/day). Protein in foods should be of high biologic value (i.e., contain a high proportion of essential amino acids). Adequate protein and calories should be provided so the patient's muscle mass is not catabolized [25].

The two leading causes of ESRD are diabetes (44% of new patients) and hypertension (29% of new cases) [59]. New cases of ESRD with diabetes or hypertension listed as the primary cause had been rising rapidly since 1980, but each has declined from 2010 to 2013 [60,61]. However, in 2019, 60.6% of those with ESRD had comorbid diabetes [138]. Approximately 6% of those with CKD and diabetes were hospitalized in 2020 [139]. Other less common causes of ESRD include glomerulonephritis, interstitial nephritis, autosomal dominant polycystic kidney disease (the leading genetic cause), and collagen vascular disease. Due to the prevalence of kidney transplantation, post-transplantation kidney disease has become the fourth largest cause of ESRD in the United States; however, these patients are reported within their original disease category for epidemiologic purposes [62]. New cases of diabetic ESRD are expectedly higher with increasing age in all racial groups, but generally stable or only slightly higher among younger individuals [63]. Statistically, non-White individuals are four times more likely to require dialysis. Compared with White patients, the prevalence of ESRD per million is 9.5 times greater in Native Hawaiians/Pacific Islanders, 3.7 times greater in Black/African Americans, 1.5 times greater in American Indians/Alaska Natives, and 1.3 times greater in Asian Americans [63]. The cost of treating ESRD was $35.4 billion in 2016 [63].

The two leading causes of ESRD are diabetes (44% of new patients) and hypertension (29% of new cases) [59]. New cases of ESRD with diabetes or hypertension listed as the primary cause had been rising rapidly since 1980, but each has declined from 2010 to 2013 [60,61]. However, in 2019, 60.6% of those with ESRD had comorbid diabetes [138]. Approximately 6% of those with CKD and diabetes were hospitalized in 2020 [139]. Other less common causes of ESRD include glomerulonephritis, interstitial nephritis, autosomal dominant polycystic kidney disease (the leading genetic cause), and collagen vascular disease. Due to the prevalence of kidney transplantation, post-transplantation kidney disease has become the fourth largest cause of ESRD in the United States; however, these patients are reported within their original disease category for epidemiologic purposes [62]. New cases of diabetic ESRD are expectedly higher with increasing age in all racial groups, but generally stable or only slightly higher among younger individuals [63]. Statistically, non-White individuals are four times more likely to require dialysis. Compared with White patients, the prevalence of ESRD per million is 9.5 times greater in Native Hawaiians/Pacific Islanders, 3.7 times greater in Black/African Americans, 1.5 times greater in American Indians/Alaska Natives, and 1.3 times greater in Asian Americans [63]. The cost of treating ESRD was $35.4 billion in 2016 [63].

An intensive and multifactorial management approach is required for patients with renal disease in order to address all risk determinants. The mainstays of treatment are management of complications and/or comorbidities, lifestyle modification, and dialysis for patients with severe or late-stage disease. Some patients may be candidates for kidney transplant, although the wait for a non-related donor can be long. Psychosocial issues and patient education (primarily to ensure compliance with the established treatment plan) are important as well.

Emotional support and educational interventions are important nursing measures for patients with neurogenic bladder. Patients may be instructed to perform the Credé maneuver to promote bladder emptying. This consists of placing the palm of the hand on the lower part of the abdomen, over the bladder. The palm of the hand is flattened, gradually increasing pressure as the palm is rotated [28].

A renal abscess is an infection that develops within the kidney. Single or multiple sites of bacterial abscess may be present. Renal abscesses are most common in patients with a history of pyelonephritis, chronic obstruction, or calculous disease [84,86,87].

Painless hematuria is the primary clinical manifestation of bladder cancer. The hematuria is typically intermittent, so it may be ignored initially. Obstruction of the urinary tract may alter the outflow of urine, causing intermittent anuria/polyuria, a decrease in the force or volume of the urinary stream, and potentially bladder distention. Infection may cause symptoms of dysuria, such as burning, frequency, or urgency [84,87,90].

Most calculi originate in the renal parenchyma (nephrolithiasis) and are passed out into the ureters or bladder (urolithiasis). Calculi are usually composed of calcium salts (calcium oxalate or phosphate, uric acid, or struvite [magnesium ammonium phosphate]). A number of factors contribute to the formation of calculi, primarily the degree to which the urine is supersaturated with a normally excreted element, the pH of the urine, the presence of substances that inhibit the formation of crystals, the stasis of urine, and the pre-existing environment [18; 86].

Gross or microscopic hematuria, flank pain, and abdominal pain are the most common manifestations of renal trauma. A significant hematoma may develop in the retroperitoneal space. Blood clots that form and descend into the ureter may result in pain that mimics renal colic and obstruction from nephrolithiasis/urolithiasis [88].

AV fistulas are not without complications, and the overall patency rate is only 50% after five years [98]. Fistula failure can be classified as early (in the first three months) or late (after three months) [98]. Early failure is generally due to infection, stenosis, or obstruction (either of inflow or outflow). Late failure is generally due to either venous stenosis or arterial lesions, with venous stenosis being the most common cause of late AV fistula failure [55,98]. Steal syndrome is another possible complication of AV fistulas and results in too high of a diversion of blood flow from the extremity distal to the fistula. Patients with steal syndrome may present with signs and symptoms of decreased blood flow to the affected extremity, particularly in the digits of the hand. Treatment of this complication includes the takedown of the fistula or placement of coils in the fistula to decrease diversion. Patients deemed at risk for imminent limb or digit loss should be referred immediately to the emergency department for evaluation by a vascular surgeon.

Cramping is also common, especially at the end of the dialysis session after large amounts of fluid and electrolytes have been removed. Severe cramping may require administration of normal saline. For patients who are significantly bothered by cramping, hydromorphone (Dilaudid) 1–2 mg orally may be given one hour before the usual onset of cramping. Hydromorphone has the advantage of not being dialyzed out of the patient's system.

Immediate postoperative care of the patient post-transplant involves all the usual issues involved in major surgery (e.g., bleeding, pain management, bowel function, infection, postoperative cardiac or pulmonary complications) as well as issues specific to kidney transplantation. These issues include graft function, acute rejection, urine leakage from the ureter anastomoses, and complications from immunosuppression. Acute rejection is not nearly the problem it was prior to the development of tacrolimus and cyclosporine, although chronic rejection remains a problem in long-term graft survival.

An end-of-life discussion is recommended in the presence of stage 4 or 5 chronic kidney disease or ESRD [114,115,116]. Hospice is generally approved when patients with ESRD are not candidates for dialysis, have a creatinine clearance less than 15 mL/minute, and/or have a serum creatinine level greater than 8 mg/dL (or 6 mg/dL in patients with diabetes) [117]. Guidelines from the Renal Physicians Association note that prognosis should be fully discussed with all patients who have stage 4 or 5 disease or ESRD [115]. Clinicians should carefully prepare for the discussion of prognosis by reviewing the patient's medical record and talking to other healthcare professionals involved in the care of the patient [118]. Because there is variation among patients regarding their desire for information, clinicians should follow the "ask-tell-ask" approach: ask the patient if he or she is willing to discuss prognosis; if yes, discuss the prognosis and then ask the patient to confirm his or her understanding [114,119]. When discussing prognosis, quantitative estimates are more understandable for patients and families than qualitative ones (e.g., "poor"), and general timeframes for survival should be given [114,119,120,121]. In addition, clinicians should emphasize that prognosis is determined by looking at large groups of patients, and that it is harder to predict survival for an individual [114,115]. The discussion of prognosis is often not documented in the patient's record, but it should be [118].