The symptoms of reflux nephropathy are comparable to nephrotic syndrome and infection of the urinary tract, though some individuals may not exhibit any evidence (symptom) of reflux nephropathy.

The underlying calyces lose their normal concave shape and show clubbing.

Renal failure is defined by functional impairment of the kidney. Renal failure can be acute or chronic, and can be further broken down into categories of pre-renal, intrinsic renal and post-renal.

Pre-renal failure refers to impairment of supply of blood to the functional nephrons including renal artery stenosis. Intrinsic renal diseases are the classic diseases of the kidney including drug toxicity and nephritis. Post-renal failure is outlet obstruction after the kidney, such as a kidney stone or prostatic bladder outlet obstruction.

Renal failure may require medication, dietary and lifestyle modification and dialysis.

Primary renal cell carcinomas as well as metastatic cancers can affect the kidney.

Urologic disease can involve congenital or acquired dysfunction of the urinary system.

Kidney diseases are normally investigated and treated by nephrologists, while the specialty of urology deals with problems in the other organs. Gynecologists may deal with problems of incontinence in women.

Diseases of other bodily systems also have a direct effect on urogenital function. For instance, it has been shown that protein released by the kidneys in diabetes mellitus sensitises the kidney to the damaging effects of hypertension.

Diabetes also can have a direct effect on urination due to peripheral neuropathies which occur in some individuals with poorly controlled diabetics.

The signs and symptoms of hydronephrosis depend upon whether the obstruction is acute or chronic, partial or complete, unilateral or bilateral. Hydronephrosis that occurs acutely with sudden onset (as caused by a kidney stone) can cause intense pain in the flank area (between the hips and ribs). Historically, this type of pain has been described as "Dietl's crisis". Conversely, hydronephrosis that develops gradually will generally cause either attacks of a dull discomfort or no pain. Nausea and vomiting may also occur. An obstruction that occurs at the urethra or bladder outlet can cause pain and pressure resulting from distension of the bladder. Blocking the flow of urine will commonly result in urinary tract infections which can lead to the development of additional stones, fever, and blood or pus in the urine. If complete obstruction occurs, kidney failure may follow.

Blood tests may show impaired kidney function (elevated urea or creatinine) or electrolyte imbalances such as hyponatremia or hyperchloremic metabolic acidosis. Urinalysis may indicate an elevated pH due to the secondary destruction of nephrons within the affected kidney. Physical examination may detect a palpable abdominal or flank mass caused by the enlarged kidney.

The prognosis of hydronephrosis is extremely variable, and depends on the condition leading to hydronephrosis, whether one (unilateral) or both (bilateral) kidneys are affected, the pre-existing kidney function, the duration of hydronephrosis (acute or chronic), and whether hydronephrosis occurred in developing or mature kidneys.

For example, unilateral hydronephrosis caused by an obstructing stone will likely resolve when the stone passes, and the likelihood of recovery is excellent. Alternately, severe bilateral prenatal hydronephrosis (such as occurs with posterior urethral valves) will likely carry a poor long-term prognosis, because obstruction while the kidneys are developing causes permanent kidney damage even if the obstruction is relieved postnatally.

Hydronephrosis can be a cause of pyonephrosis - which is a urological emergency.

Acute uric acid nephropathy is caused by deposition of uric acid crystals within the kidney interstitium and tubules, leading to partial or complete obstruction of collecting ducts, renal pelvis, or ureter. This obstruction is usually bilateral, and patients follow the clinical course of acute renal failure.

It is thought to be congenital or the consequence of vesicoureteral reflux.

The picture of acute renal failure is observed: decreased urine production and rapidly rising serum creatinine levels. Acute uric acid nephropathy is differentiated from other forms of acute renal failure by the finding of a urine uric acid/creatinine ratio > 1 in a random urine sample.

Ask-Upmark kidneys are a cause of secondary hypertension that can be curable.

In patients with this condition, the central portion of the kidney may be found just inferior to the inferior mesenteric artery because the normal embryologic ascent of the kidneys is arrested by its presence in people with central fusion of the kidneys. Horseshoe kidney is often asymptomatic, though persons affected by this condition may experience nausea, abdominal discomfort, kidney stones and urinary tract infections at greater frequency than those without renal fusion. There is currently no treatment for renal fusion other than symptomatic treatment.

Imaging Findings -

The 2 kidneys on opposite sides of the body with the lower poles fused in midline. Midline or symmetrical fusion (90% of cases).

May be missed on US, therefore pay careful attention to identification of lower poles of kidneys.

Renal long axis medially orientated,

Lower poles with curved configuration, elongation and poorly defined

Isthmus crosses midline anterior to spine and great vessels.

US for diagnosis in utero

IVP followed by CT or scintigraphy for pre-operative assessment

Variant arterial supply -

Bilateral renal arteries,

Inferior mesenteric Artery,

Arteries arising from aorta or common iliac, internal iliac, external iliac or inferior mesenteric arteries.

The lower poles of these kidneys fuse in the midline anterior to the aorta and spine. The isthmus is usually located at L4/5 level between the aorta and IMA.

Nuclear medicine (DMSA) scan confirms horseshoe kidney with fusion of both renal lower poles.

Some general secondary causes are listed below:

- Glomerular hypertrophy/hyperfiltration

- Unilateral renal agenesis

- Morbid obesity

- Scarring due to previous injury

- Focal proliferative glomerulonephritis

- Vasculitis

- Lupus

- Toxins (pamidronate)

- Human immunodeficiency virus-associated nephropathy

- Heroin nephropathy

Focal segmental glomerulosclerosis may develop following acquired loss of nephrons from reflux nephropathy. Proteinuria is nonselective in most cases and may be in subnephrotic range (nephritic range <3.0gm/24hr) or nephritic range.

Depending on the cause it is broadly classified as:

- Primary, when no underlying cause is found; usually presents as nephrotic syndrome

- Secondary, when an underlying cause is identified; usually presents with kidney failure and proteinuria. This is actually a heterogeneous group including numerous causes such as

- Toxins and drugs such as heroin and pamidronate

- Familial forms

- Secondary to nephron loss and hyperfiltration, such as with chronic pyelonephritis and reflux, morbid obesity, diabetes mellitus

There are many other classification schemes also.

While most cases of horseshoe kidneys are asymptomatic and discovered upon autopsy, the condition may increase the risk for:

- Kidney obstruction – abnormal placement of ureter may lead to obstruction and dilation of the kidney.

- Kidney infections – associated with vesicoureteral reflux.

- Kidney stones – deviant orientation of kidneys combined with slow urine flow and kidney obstruction may lead to kidney stones.

- Kidney cancer – increased risk of renal cancer, especially Wilms' tumor, transitional cell carcinoma, and an occasional case report of carcinoid tumor. Despite increased risk, the overall risk is still relatively low.

The prevalence of horseshoe kidneys in females with Turner Syndrome is about 15%.

It can be associated with trisomy 18.

It can be associated with venous anomalies like left sided IVC 9.

Most children with vesicoureteral reflux are asymptomatic. Vesicoureteral reflux may be diagnosed as a result of further evaluation of dilation of the kidney or ureters draining urine from the kidney while in utero as well as when a sibling has VUR (though routine testing in either circumstance is controversial). Reflux also increases risk of acute bladder and kidney infections, so testing for reflux may be performed after a child has one or more infections.

In infants, the signs and symptoms of a urinary tract infection may include only fever and lethargy, with poor appetite and sometimes foul-smelling urine, while older children typically present with discomfort or pain with urination and frequent urination.

Prenatally diagnosed hydronephrosis (fluid-filled kidneys) suggest post-natal follow-up examination.

The strongest neo-natal presentation is urinary tract infection. A hydronephrotic kidney may present as a palpable abdominal mass in the newborn, and may suggest an ectopic ureter or ureterocele.

In older children, ureteral duplication may present as:

- Urinary tract infection - most commonly due to vesicoureteral reflux (flow of urine from the bladder into the ureter, rather than vice versa).

- Urinary incontinence in females occurs in cases of ectopic ureter entering the vagina, urethra or vestibule.

Signs and symptoms of acute pyelonephritis generally develop rapidly over a few hours or a day. It can cause high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back. There is often associated vomiting.

Chronic pyelonephritis causes persistent flank or abdominal pain, signs of infection (fever, unintentional weight loss, malaise, decreased appetite), lower urinary tract symptoms and blood in the urine. Chronic pyelonephritis can in addition cause fever of unknown origin. Furthermore, inflammation-related proteins can accumulate in organs and cause the condition AA amyloidosis.

Physical examination may reveal fever and tenderness at the costovertebral angle on the affected side.

Pyelonephritis that has progressed to urosepsis may be accompanied by signs of septic shock, including rapid breathing, decreased blood pressure, shivering, and occasionally delirium.

Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months or years. Early on there are typically no symptoms. Later, leg swelling, feeling tired, vomiting, loss of appetite, or confusion may develop. Complications may include heart disease, high blood pressure, bone disease, or anemia.

Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of the condition. Diagnosis is generally by blood tests to measure the glomerular filtration rate and urine tests to measure albumin. Further tests such as an ultrasound or kidney biopsy may be done to determine the underlying cause. A number of different classification systems exist.

Screening at-risk people is recommended. Initial treatments may include medications to manage blood pressure, blood sugar, and lower cholesterol. NSAIDs should be avoided. Other recommended measures include staying active and certain dietary changes. Severe disease may require hemodialysis, peritoneal dialysis, or a kidney transplant. Treatments for anemia and bone disease may also be required.

Chronic kidney disease affected about 323 million people globally in 2015. In 2015 it resulted in 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

When a diagnosis of multicystic kidney is made in utero by ultrasound, the disease is found to be bilateral in many cases. Those with bilateral disease often have other severe deformities or polysystemic malformation syndromes. In bilateral cases, the newborn has the classic characteristic of Potter's syndrome.

The bilateral condition is incompatible with survival, as the contralateral system frequently is abnormal as well. Contralateral ureteropelvic junction obstruction is found in 3% to 12% of infants with multicystic kidney and contralateral vesicoureteral reflux is seen even more often, in 18% to 43% of infants. Because the high incidence of reflux, voiding cystourethrography usually has been considered advisable in all newborns with a multicystic kidney.

CKD is initially without specific symptoms and is generally only detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

- Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin-angiotensin system, increasing one's risk of developing hypertension and/or suffering from congestive heart failure.

- Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic circulation, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost").

- Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias). Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20–25 ml/min/1.73 m, at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin.

- Erythropoietin synthesis is decreased causing anemia.

- Fluid volume overload symptoms may range from mild edema to life-threatening pulmonary edema.

- Hyperphosphatemia, due to reduced phosphate excretion, follows the decrease in glomerular filtration. Hyperphosphatemia is associated with increased cardiovascular risk, being a direct stimulus to vascular calcification. Moreover, circulating concentrations of fibroblast growth factor-23 (FGF-23) increase progressively as the renal capacity for phosphate excretion declines, but this adaptative response may also contribute to left ventricular hypertrophy and increased mortality in CKD patients.

- Hypocalcemia, due to 1,25 dihydroxyvitamin D deficiency (caused by stimulation of FGF-23 and reduction of renal mass), and resistance to the calcemic action of parathyroid hormone. Osteocytes are responsible for the increased production of FGF-23, which is a potent inhibitor of the enzyme 1-alpha-hydroxylase (responsible for the conversion of 25-hydroxycholecalciferol into 1,25 dihydroxyvitamin D). Later, this progresses to secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification that further impairs cardiac function. An extreme consequence is the occurrence of the rare condition named calciphylaxis.

- The concept of chronic kidney disease-mineral bone disorder (CKD-MBD) currently describes a broader clinical syndrome that develops as a systemic disorder of mineral and bone metabolism due to CKD manifested by either "one or a combination" of: 1) abnormalities of calcium, phosphorus (phosphate), parathyroid hormone, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and 3) vascular or other soft-tissue calcification. CKD-MBD has been associated to poor hard outcomes.

- Metabolic acidosis (due to accumulation of sulfates, phosphates, uric acid etc.) may cause altered enzyme activity by excess acid acting on enzymes; and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia). Acidosis is also due to decreased capacity to generate enough ammonia from the cells of the proximal tubule.

- Iron deficiency anemia, which increases in prevalence as kidney function decreases, is especially prevalent in those requiring haemodialysis. It is multifactoral in cause, but includes increased inflammation, reduction in erythropoietin, and hyperuricemia leading to bone marrow suppression.

People with CKD suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with CKD and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.

Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.

The American Urological Association recommends ongoing monitoring of children with VUR until the abnormality resolves or is no longer clinically significant. The recommendations are for annual evaluation of blood pressure, height, weight, analysis of the urine, and kidney ultrasound.

Duplicated ureter or Duplex Collecting System is a congenital condition in which the ureteric bud, the embryological origin of the ureter, splits (or arises twice), resulting in two ureters draining a single kidney. It is the most common renal abnormality, occurring in approximately 1% of the population. The additional ureter may result in a ureterocele, or an ectopic ureter.

Multicystic dysplastic kidney (MCDK) is a condition that results from the malformation of the kidney during fetal development. The kidney consists of irregular cysts of varying sizes. Multicystic dysplastic kidney is a common type of renal cystic disease, and it is a cause of an abdominal mass in infants.

Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.

The BUN:Cr in postrenal azotemia is initially >15. The increased nephron tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine. Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.

Pyelonephritis is inflammation of the kidney, typically due to a bacterial infection. Symptoms most often include fever and flank tenderness. Other symptoms may include nausea, burning with urination, and frequent urination. Complications may include pus around the kidney, sepsis, or kidney failure.

It is typically due to a bacterial infection, most commonly "Escherichia coli". Risk factors include sexual intercourse, prior urinary tract infections, diabetes, structural problems of the urinary tract, and spermicide use. The mechanism of infection is usually spread up the urinary tract. Less often infection occurs through the bloodstream. Diagnosis is typically based on symptoms and supported by urinalysis. If there is no improvement with treatment, medical imaging may be recommended.

Pyelonephritis may be preventable by urination after sex and drinking sufficient fluids. Once present it is generally treatment with antibiotic, such as ciprofloxacin or ceftriaxone. Those with severe disease may required treatment in hospital. In those with certain structural problems of the urinary tract or kidney stones, surgery may be required.

Pyelonephritis is common. About 1 to 2 per 1,000 women are affected a year and just under 0.5 per 1,000 males. Young adult females are most often affected, followed by the very young and old. With treatment, outcomes are generally good in young adults. Among people over the age of 65 the risk of death is about 40%.