In people with a history of stones, those who are less than 50 years of age and are presenting with the symptoms of stones without any concerning signs do not require helical CT scan imaging. A CT scan is also not typically recommended in children.

Otherwise a noncontrast helical CT scan with sections is the diagnostic modality of choice in the radiographic evaluation of suspected nephrolithiasis. All stones are detectable on CT scans except very rare stones composed of certain drug residues in the urine, such as from indinavir. Calcium-containing stones are relatively radiodense, and they can often be detected by a traditional radiograph of the abdomen that includes the kidneys, ureters, and bladder (KUB film). Some 60% of all renal stones are radiopaque. In general, calcium phosphate stones have the greatest density, followed by calcium oxalate and magnesium ammonium phosphate stones. Cystine calculi are only faintly radiodense, while uric acid stones are usually entirely radiolucent.

Where a CT scan is unavailable, an intravenous pyelogram may be performed to help confirm the diagnosis of urolithiasis. This involves intravenous injection of a contrast agent followed by a KUB film. Uroliths present in the kidneys, ureters or bladder may be better defined by the use of this contrast agent. Stones can also be detected by a retrograde pyelogram, where a similar contrast agent is injected directly into the distal ostium of the ureter (where the ureter terminates as it enters the bladder).

Renal ultrasonography can sometimes be useful, as it gives details about the presence of hydronephrosis, suggesting the stone is blocking the outflow of urine. Radiolucent stones, which do not appear on KUB, may show up on ultrasound imaging studies. Other advantages of renal ultrasonography include its low cost and absence of radiation exposure. Ultrasound imaging is useful for detecting stones in situations where X-rays or CT scans are discouraged, such as in children or pregnant women. Despite these advantages, renal ultrasonography in 2009 was not considered a substitute for noncontrast helical CT scan in the initial diagnostic evaluation of urolithiasis. The main reason for this is that compared with CT, renal ultrasonography more often fails to detect small stones (especially ureteral stones), as well as other serious disorders that could be causing the symptoms. A 2014 study confirmed that ultrasonography rather than CT as an initial diagnostic test results in less radiation exposure and did not find any significant complications.

Laboratory investigations typically carried out include:

- microscopic examination of the urine, which may show red blood cells, bacteria, leukocytes, urinary casts and crystals;

- urine culture to identify any infecting organisms present in the urinary tract and sensitivity to determine the susceptibility of these organisms to specific antibiotics;

- complete blood count, looking for neutrophilia (increased neutrophil granulocyte count) suggestive of bacterial infection, as seen in the setting of struvite stones;

- renal function tests to look for abnormally high blood calcium blood levels (hypercalcemia);

- 24 hour urine collection to measure total daily urinary volume, magnesium, sodium, uric acid, calcium, citrate, oxalate and phosphate;

- collection of stones (by urinating through a StoneScreen kidney stone collection cup or a simple tea strainer) is useful. Chemical analysis of collected stones can establish their composition, which in turn can help to guide future preventive and therapeutic management.

If a kidney stone is suspected (e.g. on the basis of characteristic colicky pain or the presence of a disproportionate amount of blood in the urine), a kidneys, ureters, and bladder x-ray (KUB film) may assist in identifying radioopaque stones. Where available, a noncontrast helical CT scan with 5 millimeter sections is the diagnostic modality of choice in the radiographic evaluation of suspected nephrolithiasis. All stones are detectable on CT scans except very rare stones composed of certain drug residues in the urine. In patients with recurrent ascending urinary tract infections, it may be necessary to exclude an anatomical abnormality, such as vesicoureteral reflux or polycystic kidney disease. Investigations used in this setting include kidney ultrasonography or voiding cystourethrography. CT scan or kidney ultrasonography is useful in the diagnosis of xanthogranulomatous pyelonephritis; serial imaging may be useful for differentiating this condition from kidney cancer.

Ultrasound findings that indicate pyelonephritis are enlargement of the kidney, edema in the renal sinus or parenchyma, bleeding, loss of corticomedullary differentiation, abscess formation, or an areas of poor blood flow on doppler ultrasound. However, ultrasound findings are seen in only 20% to 24% of people with pyelonephritis.

A DMSA scan is a radionuclide scan that uses dimercaptosuccinic acid in assessing the kidney morphology. It is now the most reliable test for the diagnosis of acute pyelonephritis.

Analysis of the urine may show signs of urinary tract infection. Specifically, the presence of nitrite and white blood cells on a urine test strip in patients with typical symptoms are sufficient for the diagnosis of pyelonephritis, and are an indication for empirical treatment. Blood tests such as a complete blood count may show neutrophilia. Microbiological culture of the urine, with or without blood cultures and antibiotic sensitivity testing are useful for establishing a formal diagnosis, and are considered mandatory.

Classically, MSK is seen as hyperdense papillae with clusters of small stones on ultrasound examination of the kidney or with an abdominal x-ray. The irregular (ectatic) collecting ducts are often seen in MSK, which are sometimes described as having a "paintbrush-like" appearance, are best seen on intravenous urography. However, IV urography has been largely replaced by contrast-enhanced, high-resolution helical CT with digital reconstruction.

The sensitivity of an abnormal gallium scan has been reported to range from 60% to 100%.

Complications of analgesic nephropathy include pyelonephritis and end-stage kidney disease. Risk factors for poor prognosis include recurrent urinary tract infection and persistently elevated blood pressure. Analgesic nephropathy also appears to increase the risk of developing cancers of the urinary system.

It is diagnosed by micturating cystography; scarring can be demonstrated by ultrasound or DMSA.

Diagnosis is traditionally based on the clinical findings above in combination with excessive analgesic use. It is estimated that between 2 and 3 kg each of phenacetin or aspirin must be consumed before evidence of analgesic nephropathy becomes clinically apparent.

Once suspected, analgesic nephropathy can be confirmed with relative accuracy using computed tomography (CT) imaging without contrast. One trial demonstrated that the appearance of papillary calcifications on CT imaging was 92% sensitive and 100% specific for the diagnosis of analgesic nephropathy.

Individuals with renal papillary necrosis due to excess use of analgesic have an elevated risk of epithelial tumors, hence a urine cytology exam is useful. In terms of imaging this condition can be identified by retrograde pyelography (RGP). The diagnosis of renal papillary necrosis is therefore done via:

The deterioration of kidney function may be signaled by a measurable decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Additionally, the ratio of BUN to creatinine is used to evaluate kidney injury. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none of them is currently established enough to replace creatinine as a marker of kidney function.

Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. It is useful to perform a bladder scan or a post void residual to rule out urinary retention. In post void residual, a catheter is inserted into the urinary tract immediately after urinating to measure fluid still in the bladder. 50–100 ml suggests neurogenic bladder dysfunction.

These may include urine sediment analysis, renal ultrasound and/or kidney biopsy. Indications for kidney biopsy in the setting of AKI include the following:

1. Unexplained AKI, in a patient with two non-obstructed normal sized kidneys

2. AKI in the presence of the nephritic syndrome

3. Systemic disease associated with AKI

4. Kidney transplant dysfunction

In medical imaging, the acute changes in the kidney are often examined with renal ultrasonography as the first-line modality, where CT scan and magnetic resonance imaging (MRI) are used for the follow-up examinations and when US fails to demonstrate abnormalities. In evaluation of the acute changes in the kidney, the echogenicity of the renal structures, the delineation of the kidney, the renal vascularity, kidney size and focal abnormalities are observed. CT is preferred in renal traumas, but US is used for follow-up, especially in the patients suspected for the formation of urinomas. A CT scan of the abdomen will also demonstrate bladder distension or hydronephrosis. However, in AKI, the use of IV contrast is contraindicated as the contrast agent used is nephrotoxic.

Urinary findings include:

- Eosinophiluria: Original studies with Methicillin-induced AIN showed sensitivity of 67% and specificity of 83%. The sensitivity is higher in patients with interstitial nephritis induced by methicillin or when the Hansel's stain is used. However, a 2013 study showed that the sensitivity and specificity of urine eosinophil testing are 35.6% and 68% respectively.

- Isosthenuria

- Blood in the urine and occasional RBC casts

- Sterile pyuria: white blood cells and no bacteria

- Nephrotic-range amount of protein in the urine may be seen with NSAID-associated AIN

Nephrocalcinosis is diagnosed for the most part by imaging techniques. The imagings used are ultrasound (US), abdominal plain film and CT imaging. Of the 3 techniques CT and US are the more preferred. Nephrocalcinosis is considered present if at least two radiologists make the diagnosis on US and/or CT. In some cases a renal biopsy is done instead if imaging is not enough to confirm nephrocalcinosis. Once the diagnosis is confirmed additional testing is needed to find the underlying cause because the underlying condition may require treatment for reasons independent of nephrocalcinosis. These additional tests will measure serum, electrolytes, calcium, and phosphate, and the urine pH. If no underlying cause can be found then urine collection should be done for 24 hours and measurements of the excretion of calcium, phosphate, oxalate, citrate, and creatinine are looked at.

The diagnosis depends on the cause of the nephritis, in the case of lupus nephritis, blood tests, X-rays and an ultrasound can help ascertain if the individual has the condition.

There is a genetic predisposition, first-degree relatives have a great increase in the chance of VUR. The gene frequency is estimated to be 1:600. The American Academy of Pediatrics recommends that children from 2 to 24 months presenting with a UTI should be investigated for VUR.

Treatment of renal papillary necrosis is supportive, any obstruction (urethral) can be dealt with via stenting. This condition is not linked to a higher possibility of renal failure. Control of infection is important, thus antimicrobial treatment is begun, so as to avert surgery (should the infection not respond).

The "RIFLE criteria", proposed by the Acute Dialysis Quality Initiative (ADQI) group, aid in assessment of the severity of a person's acute kidney injury. The acronym RIFLE is used to define the spectrum of progressive kidney injury seen in AKI:

- Risk: 1.5-fold increase in the serum creatinine, or glomerular filtration rate (GFR) decrease by 25 percent, or urine output <0.5 mL/kg per hour for six hours.

- Injury: Two-fold increase in the serum creatinine, or GFR decrease by 50 percent, or urine output <0.5 mL/kg per hour for 12 hours

- Failure: Three-fold increase in the serum creatinine, or GFR decrease by 75 percent, or urine output of <0.3 mL/kg per hour for 24 hours, or no urine output (anuria) for 12 hours

- Loss: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than four weeks

- End-stage kidney disease: Complete loss of kidney function (e.g., need for renal replacement therapy) for more than three months

Often, aggressive treatment is unnecessary for people with MSK disease that does not cause any symptoms (asymptomatic). In such cases, treatment may consist of maintaining adequate fluid intake, with the goal of decreasing the risk of developing kidney stones (nephrolithiasis). Cases of recurrent kidney stone formation may warrant evaluation for possible underlying metabolic abnormalities.

In patients with low levels of citrate in the urine (hypocitraturia) and incomplete distal renal tubular acidosis, treatment with potassium citrate helps prevent the formation of new kidney stones. Urinary tract infections, when they occur, should also be treated.

Patients with the more rare form of MSK marked by chronic pain typically require pain management. Non-obstructing stones in MSK can be associated with significant and chronic pain even if they're not passing. The pain in this situation can be constant. It is not certain what causes this pain but researchers have proposed that the small numerous stones seen in MSK may cause obstruction of the small tubules and collecting ducts in the kidney which could lead to the pain. This pain can often be debilitating and treatment is challenging. Narcotic medication even with large quantities is sometimes not adequate. Some success with pain control has been reported using laser lithotripsy (called “ureteroscopic laser papillotomy”).

Treatment/management of nephritis depends on what has provoked the inflammation of the kidney(s). In the case of lupus nephritis, hydroxychloroquine could be used.

This requires drainage, best performed by ureteral stent placement or nephrostomy.

Testing for bacteriuria is often performed in those with symptoms of a urinary tract infection. Testing is often done in other scenarios as in failure to thrive of a newborn or confusion in the elderly. Screening for bacteriuria is recommended in pregnancy as there is evidence that asymptomatic bacteriuria can lead to low birth weight and preterm delivery.

- Bacteriuria can be detected by urine dipstick test. The urinary nitrite test will be able to detect any nitrate-reducing bacteria in the urine. The leukocyte esterase test detects the presence of leukocytes (white blood cells) in the urine which can be associated with a urinary tract infection.The urine dipstick test is readily available and provides fast results.

- Microscopy can also be used to detect bacteriuria. It is more specific, especially when used with gram staining, but requires more time and equipment.

- The gold standard for detecting bacteriuria is a bacterial culture which identifies the actual organism. This test is more specific but can take several days to obtain a result. As a result, clinicians will often treat a bacteriuria based on the results of the urine dipstick test while waiting for the culture results. The culture will often provide antibiotic sensitivity.

Bacteriuria can be confirmed if a single bacterial species is isolated in a concentration greater than 100,000 colony forming units per millilitre of urine in clean-catch midstream urine specimens (one for men, two consecutive specimens with the same bacterium for women). For urine collected via bladder catheterization in men and women, a single urine specimen with greater than 100,000 colony forming units of a single species per millilitre is considered diagnostic. The threshold is also 100 colony forming units of a single species per millilitre for women displaying UTI symptoms.

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.

The decision to treat bacteriuria depends on the presence of accompany symptoms and comorbidities.

Increasing fluid intake to yield a urine output of greater than 2 liters a day can be advantageous for all patients with nephrocalcinosis. Patients with hypercalciuria can reduce calcium excretion by restricting animal protein, limiting sodium intake to less than 100 meq a day and being lax of potassium intake. If changing ones diet alone does not result in an suitable reduction of hypercalciuria, a thiazide diuretic can be administered in patients who do not have hypercalcemia. Citrate can increase the solubility of calcium in urine and limit the development of nephrocalcinosis. Citrate is not given to patients who have urine pH equal to or greater than 7.

Patients will require dialysis to compensate for the function of their kidneys.