It is possible to analyze urine samples in determining albumin, hemoglobin and myoglobin with an optimized MEKC method.

The standard diagnostic workup of suspected kidney disease is history & examination, as well as a urine test strip. Also, renal ultrasonography is essential in the diagnosis and management of kidney-related diseases.

Conventionally, proteinuria is diagnosed by a simple dipstick test, although it is possible for the test to give a false negative reading, even with nephrotic range proteinuria if the urine is dilute. False negatives may also occur if the protein in the urine is composed mainly of globulins or Bence Jones proteins because the reagent on the test strips, bromophenol blue, is highly specific for albumin. Traditionally, dipstick protein tests would be quantified by measuring the total quantity of protein in a 24-hour urine collection test, and abnormal globulins by specific requests for protein electrophoresis. Trace results may be produced in response to excretion of Tamm–Horsfall mucoprotein.

More recently developed technology detects human serum albumin (HSA) through the use of liquid crystals (LCs). The presence of HSA molecules disrupts the LCs supported on the AHSA-decorated slides thereby producing bright optical signals which are easily distinguishable. Using this assay, concentrations of HSA as low as 15 µg/mL can be detected.

Alternatively, the concentration of protein in the urine may be compared to the creatinine level in a spot urine sample. This is termed the protein/creatinine ratio. The 2005 UK Chronic Kidney Disease guidelines states protein/creatinine ratio is a better test than 24-hour urinary protein measurement. Proteinuria is defined as a protein/creatinine ratio greater than 45 mg/mmol (which is equivalent to albumin/creatinine ratio of greater than 30 mg/mmol or approximately 300 mg/g) with very high levels of proteinuria having a ratio greater than 100 mg/mmol.

Protein dipstick measurements should not be confused with the amount of protein detected on a test for microalbuminuria which denotes values for protein for urine in mg/day versus urine protein dipstick values which denote values for protein in mg/dL. That is, there is a basal level of proteinuria that can occur below 30 mg/day which is considered non-pathology. Values between 30–300 mg/day are termed microalbuminuria which is considered pathologic. Urine protein lab values for microalbumin of >30 mg/day correspond to a detection level within the "trace" to "1+" range of a urine dipstick protein assay. Therefore, positive indication of any protein detected on a urine dipstick assay obviates any need to perform a urine microalbumin test as the upper limit for microalbuminuria has already been exceeded.

Kidney disease is a non-communicable disease, having serious consequences if it cannot be controlled effectively. Generally, the process of kidney disease development is from light to serious. Some kidney diseases can cause renal failure.

Osmotic nephrosis refers to structural changes that occur at the cellular level in the human kidney. Cells, primarily of the straight proximal tubule, swell due to the formation of large vacuoles in the cytoplasm. These vacuoles occur in the presence of large amounts of certain solutes circulating in the tubules. However, despite the condition's name, the solutes do not cause change through osmotic forces but through pinocytosis. Once inside the cytoplasm, pinocytic vacuoles combine with each other and with lysosomes to form large vacuoles that appear transparent under microscopic examination.

There may be no symptomatic presentation with this condition, or it may confused with other nephrotic conditions such as Tubular calcineurin-inhibitor toxicity. Affected cells of the proximal tubule may be passed in the urine, but a kidney biopsy is the only sure way to make a diagnosis.

Responsible exogenous solutes include sucrose-containing IVIg, mannitol, dextran, contrast dye, and hydroxyethyl starch. Prevention includes standard preventions for iatrogenic kidney damage. Osmotic nephrosis is usually reversible but can lead to chronic renal failure.

Minimal change disease has been called by many other names in the medical literature, including minimal change nephropathy, minimal change nephrosis, minimal change nephrotic syndrome, minimal change glomerulopathy, foot process disease (referring to the foot processes of the podocytes), nil disease (referring to the lack of pathologic findings on light microscopy), nil lesions, lipid nephrosis, and lipoid nephrosis.

Minimal change disease is most common in very young children but can occur in older children and adults. It is by far the most common cause of nephrotic syndrome in children between the ages of 1 and 7, accounting for the majority (about 90%) of these diagnoses. Among teenagers who develop nephrotic syndrome, it is caused by minimal change disease about half the time. It can also occur in adults but accounts for less than 20% of adults diagnosed with nephrotic syndrome. Among children less than 10 years of age, boys seem to be more likely to develop minimal change disease than girls. Minimal change disease is being seen with increasing frequency in adults over the age of 80.

People with one or more autoimmune disorders are at increased risk of developing minimal change disease. Having minimal change disease also increases the chances of developing other autoimmune disorders.

Nephrosis is any of various forms of kidney disease (nephropathy). In an old and broad sense of the term, it is any nephropathy, but in current usage the term is usually restricted to a narrower sense of nephropathy without inflammation or neoplasia, in which sense it is distinguished from nephritis, which involves inflammation. It is also defined as any purely degenerative disease of the renal tubules. Nephrosis is characterized by a set of signs called the nephrotic syndrome. Nephrosis can be a primary disorder or can be secondary to another disorder. Nephrotic complications of another disorder can coexist with nephritic complications. In other words, nephrosis and nephritis can be pathophysiologically contradistinguished, but that does not mean that they cannot occur simultaneously.

Types of nephrosis include amyloid nephrosis and osmotic nephrosis.

The history, physical exam, and laboratory testing are required to determine the underlying cause of hyponatremia. A blood test demonstrating a serum sodium less than 135 mmol/L is diagnostic for hyponatremia. The history and physical exam are necessary to help determine if the patient is hypovolemic, euvolemic, or hypervolemic, which has important implications in determining the underlying cause. An assessment is also made to determine if the patient is experiencing symptoms from their hyponatremia. These include assessments of alertness, concentration, and orientation.

Glomerulonephrosis is a non-inflammatory disease of the kidney (nephrosis) presenting primarily in the glomerulus (a glomerulopathy).

It can be contrasted to glomerulonephritis, which implies inflammation.

It can be caused by diethylnitrosamine.

False hyponatremia, also known as spurious, pseudo, hypertonic, or artifactual hyponatremia is when the lab tests read low sodium levels but there is no hypotonicity. In hypertonic hyponatremia, resorption of water by molecules such as glucose (hyperglycemia or diabetes) or mannitol (hypertonic infusion) occurs. In isotonic hyponatremia a measurement error due to high blood triglyceride level (most common) or paraproteinemia occurs. It occurs when using techniques that measure the amount of sodium in a specified volume of serum/plasma, or that dilute the sample before analysis.

Daentl Townsend Siegel syndrome is a very rare disorder characterized by blue sclerae, kidney malfunction, thin skin, and hydrocephalus. It was first identified by D.L. Daentl et al. in 1978. Daentl Townsend Siegel syndrome is also known as "Hydrocephalus blue sclera nephropathy" and "Familial nephrosis, hydrocephalus, thin skin, blue sclerae syndrome".