Uremic neuropathy is a symmetric, mixed sensorimotor neuropathy, with longer axons being affected first. It afflicts most patients with end-stage renal disease; uremic toxins are thought to be the major contributors to the disease. Dialysis may stabilize the disease, but the most successful treatment is renal transplantation.
Among the types of neuropathy associated with uremia, polyneuropathy is the most characteristic, but focal and shunt-related neuropathies also occur . The neuropathy only develops in patients who have substantially decreased glomerular filtration rates (less than 12 ml/min) , and was found in early studies using nerve biopsies to progress from distal to proximal sites . It affects the lower extremities to a larger extent than the upper, and males more than females. The primary defect is axonal degeneration, accompanied by secondary segmental demyelination .
The early symptoms show mainly sensory losses, but motor function is also affected. The earliest signs include the loss of the Achilles reflex . This and other early signs, - such as paresthesias, reduction in vibration sense and deep tendon reflexes, perturbation of position sensation, and muscle weakness - indicate defects in large fibers. Damage to small fibers can also show up as allodynia, pain, changes in temperature sensation, and visceral pain.
Uremic neuropathy needs to be differentiated from other forms of peripheral neuropathy. Foremost among these is diabetic neuropathy, as diabetes is often the cause of chronic kidney disease  ; however, there are other metabolic and hormonal states, as well as vitamin deficiencies, toxins, and inflammatory conditions that can cause neuropathies. Blood tests can be used for the identification of vitamin deficiencies (for example B12) and diabetes. They can also be used to detect antinuclear antibodies, markers of inflammation, and hormone levels.
Some of the neuropathies that need to be ruled out are vasculitic neuropathy , chronic or acute demyelinating neuropathies, such as the Guillain-Barré syndrome, and inflammatory demyelinating neuropathies associated with membranous glomerulonephritis  .
After general and neurological examinations, which provide background information, electrodiagnostic tools – sensory and motor nerve conduction, F response, H reflex and needle electromyography - help in categorizing the deficit, and defining its extent. . These methods can also distinguish between axonal degeneration and demyelination, and characterize the disease as polyneuropathy or mononeuropathy .
Early studies of uremic neuropathy measured nerve conduction velocities and found them to be decreased, even in patients without clinical symptoms. Subsequent studies also found general slowing and abnormalities in conductance, but in addition noted a decrease in the amplitude in sensory, but not motor responses . In one recent study, the amplitude of the sural sensory nerve action potential was the parameter most commonly affected in patients with end-stage kidney disease . Another recent study also found sural sensory action potential a sensitive predictor of neuropathy, but identified F wave latency as the most sensitive indicator, especially in subclinical polyneuropathy .
Nerve excitability measurements, which identify changes in axonal membrane potential in neuropathy , were also performed on patients with chronic kidney disease . These studies showed a reduction in compound muscle action potential, and indicated that axonal membranes were depolarized . The excitability markers showed noticeable improvement on dialysis, and thus may be a good indication regarding the adequacy of dialysis . More than one study   detected a correlation between potassium levels and excitability markers, and concluded that it may be important to maintain normal serum potassium concentration between courses of dialysis .