Immune
Variations in genes that are part of the immune system or part of melanocytes have both been associated with vitiligo. It is also thought to be caused by the immune system attacking and destroying the melanocytes of the skin. A genome wide association study found approximately 36 independent susceptibility loci for generalized vitiligo. Autoimmune associations
Vitiligo is sometimes associated with autoimmune and inflammatory diseases such as Hashimotos thyroiditis, scleroderma, rheumatoid arthritis, type 1 diabetes mellitus, psoriasis, Addisons disease, pernicious anemia, alopecia areata, systemic lupus erythematosus, and celiac disease.Among the inflammatory products of NALP1 are caspase 1 and caspase 7, which activate the inflammatory cytokine interleukin-1β. Interleukin-1β and interleukin-18 are expressed at high levels in people with vitiligo. In one of the mutations, the amino acid leucine in the NALP1 protein was replaced by histidine (Leu155 → His). The original protein and sequence is highly conserved in evolution, and is found in humans, chimpanzee, rhesus monkey, and the bush baby. Addisons disease (typically an autoimmune destruction of the adrenal glands) may also be seen in individuals with vitiligo. Diagnosis
An ultraviolet light can be used in the early phase of this disease for identification and to determine the effectiveness of treatment. Using a Woods light, skin will change colour (fluoresce) when it is affected by certain bacteria, fungi, and changes to pigmentation of the skin. Classification
Classification attempts to quantify vitiligo have been analyzed as being somewhat inconsistent, while recent consensus have agreed to a system of segmental vitiligo (SV) and non-segmental vitiligo (NSV).
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. Pathophysiology
Ureteral development begins in the human fetus around the 4th week of embryonic development. A ureteric bud, arising from the mesonephric (or Wolffian) duct, gives rise to the ureter, as well as other parts of the collective system. In the case of a duplicated ureter, the ureteric bud either splits or arises twice. In most cases, the kidney is divided into two parts, an upper and lower lobe, with some overlap due to intermingling of collecting tubules. However, in some cases the division is so complete as to give rise to two separate parts, each with its own renal pelvis and ureter. Diagnosis
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. Classification
Ureteral duplication is either of:

Partial
I.e., the two ureters drain into the bladder via a single common ureter.