Medulla In Patients Research Articles

Acquired Renal Cystic Disease Mimicking Adult Polycystic Kidney Disease in a Patient Undergoing Long-Term Hemodialysis

Acquired renal cystic disease (ARCD) is defined as the development of multiple cysts in the renal cortex and medulla in patients with chronic renal failure who are free from congenital polycystic kidney disease. ARCD develops generally in contracted kidneys. We report a case of grotesque enlargement of a single kidney in a patient who had been receiving hemodialysis for 18 years. Although the exact causes of ARCD are not known, 3 factors may contribute to the development of nephromegaly; the sex, the duration of hemodialysis and previous unilateral nephrectomy. As in polycystic disease, when the involved kidney reaches considerable size, ARCD may have a favorable effect on anemia caused by chronic renal failure.

Disturbed function of the pineal gland in familial amyloid polyneuropathy

In order to estimate the function of the pineal gland, the sympathetic nervous system and the adrenal medulla in patients with familial amyloid polyneuropathy relative to healthy subjects, we have quantified urinary 6-hydroxymelatonin, normetanephrine and metanephrine. Urinary 6-hydroxymelatonin level correlated with neither of two O-methylated catecholamine levels in healthy subjects. The excretion of both 6-hydroxymelatonin and metanephrine were reduced in the patient group as compared with the control group, and the normal daily rhythm of 6-hydroxymelatonin was undetectable in the most of the patients. This finding indicates that the function of the pineal gland is disturbed in familial amyloid polyneuropathy.

Depletion of substance P-containing axons in substantia gelatinosa of patients with diminished pain sensitivity.

Substance P is an undecapeptide which may be involved in transmission of nociceptive information at synapses of primary sensory neurones1,2. It occurs in 10–20% of rat dorsal root ganglion neurones3,4. Small substance P-immunoreactive (SP-IR) axons from dorsal root ganglia enter the spinal cord and form a dense terminal network in the substantia gelatinosa of the rat dorsal horn3; analogous fibres from the trigeminal ganglion terminate in the substantia gelatinosa of the spinal trigeminal tract of the medulla oblongata4,5, while sensory axons travelling via the petrosal and nodose ganglia terminate in the tractus solitarius of the medulla5–8. Substance P is also present in human spinal cord and pallido-nigral system9–12. In addition to sympathetic and parasympathetic abnormalities, patients with familial dysautonomia (the Riley–Day syndrome) have severe diminution of temperature and pain sensitivity, reduced populations of primary sensory neurones and small Lissauer's tracts13. It was thus postulated that a diminution of primary substance P axons might be demonstrable using immunocytochemistry. We report here the presence of anatomically discrete depletion of substance P immunoreactivity in the substantia gelatinosa of spinal cord and medulla of patients with familial dysautonomia. The results are consistent with the hypothesis that substance P is involved in the transmission of impulses related to pain.